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  • Articles  (776)
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  • 1
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    The inside story on wearable electronics (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibney, Elizabeth -- England -- Nature. 2015 Dec 3;528(7580):26-8. doi: 10.1038/528026a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26632572" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bioengineering/instrumentation/methods ; Clothing ; *Early Diagnosis ; Electronics/*instrumentation ; *Equipment Design ; Humans ; Monitoring, Physiologic/*instrumentation/*methods ; Myocardial Infarction/diagnosis/drug therapy/prevention & control ; Rats ; Seizures/diagnosis/drug therapy/prevention & control ; *Transdermal Patch
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Surgeon commits misconduct (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-05-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cyranoski, David -- England -- Nature. 2015 May 28;521(7553):406-7. doi: 10.1038/nature.2015.17605.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26017424" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bioartificial Organs ; Esophagus/surgery ; Humans ; Rats ; Research Personnel/*ethics ; *Scientific Misconduct/legislation & jurisprudence ; Stem Cell Transplantation/ethics ; Surgeons/*ethics ; Sweden ; Trachea/*surgery
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Conformational dynamics of a class C G-protein-coupled receptor (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-08-11
    Description: G-protein-coupled receptors (GPCRs) constitute the largest family of membrane receptors in eukaryotes. Crystal structures have provided insight into GPCR interactions with ligands and G proteins, but our understanding of the conformational dynamics of activation is incomplete. Metabotropic glutamate receptors (mGluRs) are dimeric class C GPCRs that modulate neuronal excitability, synaptic plasticity, and serve as drug targets for neurological disorders. A 'clamshell' ligand-binding domain (LBD), which contains the ligand-binding site, is coupled to the transmembrane domain via a cysteine-rich domain, and LBD closure seems to be the first step in activation. Crystal structures of isolated mGluR LBD dimers led to the suggestion that activation also involves a reorientation of the dimer interface from a 'relaxed' to an 'active' state, but the relationship between ligand binding, LBD closure and dimer interface rearrangement in activation remains unclear. Here we use single-molecule fluorescence resonance energy transfer to probe the activation mechanism of full-length mammalian group II mGluRs. We show that the LBDs interconvert between three conformations: resting, activated and a short-lived intermediate state. Orthosteric agonists induce transitions between these conformational states, with efficacy determined by occupancy of the active conformation. Unlike mGluR2, mGluR3 displays basal dynamics, which are Ca(2+)-dependent and lead to basal protein activation. Our results support a general mechanism for the activation of mGluRs in which agonist binding induces closure of the LBDs, followed by dimer interface reorientation. Our experimental strategy should be widely applicable to study conformational dynamics in GPCRs and other membrane proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4597782/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4597782/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vafabakhsh, Reza -- Levitz, Joshua -- Isacoff, Ehud Y -- 2PN2EY018241/EY/NEI NIH HHS/ -- PN2 EY018241/EY/NEI NIH HHS/ -- England -- Nature. 2015 Aug 27;524(7566):497-501. doi: 10.1038/nature14679. Epub 2015 Aug 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA. ; Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720, USA. ; Physical Bioscience Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26258295" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Drug Partial Agonism ; *Fluorescence Resonance Energy Transfer ; Humans ; Ligands ; Models, Biological ; Models, Molecular ; Protein Binding ; Protein Conformation ; Rats ; Receptors, Metabotropic Glutamate/*chemistry/*classification/genetics/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Optogenetic control of organelle transport and positioning (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-01-07
    Description: Proper positioning of organelles by cytoskeleton-based motor proteins underlies cellular events such as signalling, polarization and growth. For many organelles, however, the precise connection between position and function has remained unclear, because strategies to control intracellular organelle positioning with spatiotemporal precision are lacking. Here we establish optical control of intracellular transport by using light-sensitive heterodimerization to recruit specific cytoskeletal motor proteins (kinesin, dynein or myosin) to selected cargoes. We demonstrate that the motility of peroxisomes, recycling endosomes and mitochondria can be locally and repeatedly induced or stopped, allowing rapid organelle repositioning. We applied this approach in primary rat hippocampal neurons to test how local positioning of recycling endosomes contributes to axon outgrowth and found that dynein-driven removal of endosomes from axonal growth cones reversibly suppressed axon growth, whereas kinesin-driven endosome enrichment enhanced growth. Our strategy for optogenetic control of organelle positioning will be widely applicable to explore site-specific organelle functions in different model systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Bergeijk, Petra -- Adrian, Max -- Hoogenraad, Casper C -- Kapitein, Lukas C -- England -- Nature. 2015 Feb 5;518(7537):111-4. doi: 10.1038/nature14128. Epub 2015 Jan 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology, Department of Biology, Faculty of Science, Utrecht University, 3584 CH Utrecht, The Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25561173" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology/radiation effects ; Biological Transport/radiation effects ; Cell Compartmentation/*physiology/radiation effects ; Cells, Cultured ; Cytoskeleton/metabolism/radiation effects ; Dendritic Spines/metabolism/radiation effects ; Dyneins/metabolism/radiation effects ; Endosomes/*metabolism/radiation effects ; Hippocampus/cytology ; Intracellular Space/metabolism/radiation effects ; Kinesin/metabolism/radiation effects ; Microtubules/metabolism/radiation effects ; Mitochondria/*metabolism/radiation effects ; Myosin Type V/metabolism/radiation effects ; Optogenetics/*methods ; Peroxisomes/*metabolism/radiation effects ; Rats
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    alpha-Synuclein strains cause distinct synucleinopathies after local and systemic administration (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-06-11
    Description: Misfolded protein aggregates represent a continuum with overlapping features in neurodegenerative diseases, but differences in protein components and affected brain regions. The molecular hallmark of synucleinopathies such as Parkinson's disease, dementia with Lewy bodies and multiple system atrophy are megadalton alpha-synuclein-rich deposits suggestive of one molecular event causing distinct disease phenotypes. Glial alpha-synuclein (alpha-SYN) filamentous deposits are prominent in multiple system atrophy and neuronal alpha-SYN inclusions are found in Parkinson's disease and dementia with Lewy bodies. The discovery of alpha-SYN assemblies with different structural characteristics or 'strains' has led to the hypothesis that strains could account for the different clinico-pathological traits within synucleinopathies. In this study we show that alpha-SYN strain conformation and seeding propensity lead to distinct histopathological and behavioural phenotypes. We assess the properties of structurally well-defined alpha-SYN assemblies (oligomers, ribbons and fibrils) after injection in rat brain. We prove that alpha-SYN strains amplify in vivo. Fibrils seem to be the major toxic strain, resulting in progressive motor impairment and cell death, whereas ribbons cause a distinct histopathological phenotype displaying Parkinson's disease and multiple system atrophy traits. Additionally, we show that alpha-SYN assemblies cross the blood-brain barrier and distribute to the central nervous system after intravenous injection. Our results demonstrate that distinct alpha-SYN strains display differential seeding capacities, inducing strain-specific pathology and neurotoxic phenotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peelaerts, W -- Bousset, L -- Van der Perren, A -- Moskalyuk, A -- Pulizzi, R -- Giugliano, M -- Van den Haute, C -- Melki, R -- Baekelandt, V -- England -- Nature. 2015 Jun 18;522(7556):340-4. doi: 10.1038/nature14547. Epub 2015 Jun 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉KU Leuven, Laboratory for Neurobiology and Gene Therapy, Department of Neurosciences, 3000 Leuven, Belgium. ; Paris-Saclay Institute of Neuroscience, CNRS, Avenue de la Terrasse, 91198 Gif-sur-Yvette, France. ; Theoretical Neurobiology &Neuroengineering Laboratory, Department of Biomedical Sciences, University of Antwerp, 2610 Antwerp, Belgium. ; 1] Theoretical Neurobiology &Neuroengineering Laboratory, Department of Biomedical Sciences, University of Antwerp, 2610 Antwerp, Belgium [2] Department of Computer Science, University of Sheffield, S1 4DP Sheffield, UK [3] Brain Mind Institute, Swiss Federal Institute of Technology of Lausanne, 1015 Lausanne, Switzerland [4] Neuro-Electronics Research Flanders (NERF), 3001 Leuven, Belgium. ; 1] KU Leuven, Laboratory for Neurobiology and Gene Therapy, Department of Neurosciences, 3000 Leuven, Belgium [2] KU Leuven, Leuven Viral Vector Core, 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26061766" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood-Brain Barrier ; Brain/drug effects/metabolism ; Female ; Humans ; Lewy Body Disease/*chemically induced/metabolism/pathology ; Multiple System Atrophy/*chemically induced/metabolism/pathology ; Parkinson Disease/metabolism/*pathology ; Phenotype ; Rats ; Rats, Wistar ; Substantia Nigra/drug effects/metabolism/pathology ; Synapses/metabolism/pathology ; alpha-Synuclein/*administration & dosage/chemistry/classification/*toxicity
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  • 6
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    The zinc transporter ZIP12 regulates the pulmonary vascular response to chronic hypoxia (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-08-11
    Description: The typical response of the adult mammalian pulmonary circulation to a low oxygen environment is vasoconstriction and structural remodelling of pulmonary arterioles, leading to chronic elevation of pulmonary artery pressure (pulmonary hypertension) and right ventricular hypertrophy. Some mammals, however, exhibit genetic resistance to hypoxia-induced pulmonary hypertension. We used a congenic breeding program and comparative genomics to exploit this variation in the rat and identified the gene Slc39a12 as a major regulator of hypoxia-induced pulmonary vascular remodelling. Slc39a12 encodes the zinc transporter ZIP12. Here we report that ZIP12 expression is increased in many cell types, including endothelial, smooth muscle and interstitial cells, in the remodelled pulmonary arterioles of rats, cows and humans susceptible to hypoxia-induced pulmonary hypertension. We show that ZIP12 expression in pulmonary vascular smooth muscle cells is hypoxia dependent and that targeted inhibition of ZIP12 inhibits the rise in intracellular labile zinc in hypoxia-exposed pulmonary vascular smooth muscle cells and their proliferation in culture. We demonstrate that genetic disruption of ZIP12 expression attenuates the development of pulmonary hypertension in rats housed in a hypoxic atmosphere. This new and unexpected insight into the fundamental role of a zinc transporter in mammalian pulmonary vascular homeostasis suggests a new drug target for the pharmacological management of pulmonary hypertension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Lan -- Oliver, Eduardo -- Maratou, Klio -- Atanur, Santosh S -- Dubois, Olivier D -- Cotroneo, Emanuele -- Chen, Chien-Nien -- Wang, Lei -- Arce, Cristina -- Chabosseau, Pauline L -- Ponsa-Cobas, Joan -- Frid, Maria G -- Moyon, Benjamin -- Webster, Zoe -- Aldashev, Almaz -- Ferrer, Jorge -- Rutter, Guy A -- Stenmark, Kurt R -- Aitman, Timothy J -- Wilkins, Martin R -- 098424/Wellcome Trust/United Kingdom -- 101033/Wellcome Trust/United Kingdom -- MR/J0003042/1/Medical Research Council/United Kingdom -- P01 HL014985/HL/NHLBI NIH HHS/ -- PG/04/035/16912/British Heart Foundation/United Kingdom -- PG/10/59/28478/British Heart Foundation/United Kingdom -- PG/12/61/29818/British Heart Foundation/United Kingdom -- PG/2000137/British Heart Foundation/United Kingdom -- PG/95170/British Heart Foundation/United Kingdom -- PG/98018/British Heart Foundation/United Kingdom -- RG/10/16/28575/British Heart Foundation/United Kingdom -- WT098424AIA/Wellcome Trust/United Kingdom -- England -- Nature. 2015 Aug 20;524(7565):356-60. doi: 10.1038/nature14620. Epub 2015 Aug 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Pharmacology and Therapeutics, Division of Experimental Medicine, Imperial College London, Hammersmith Hospital, London W12 0NN, UK. ; Physiological Genomics and Medicine Group, Medical Research Council Clinical Sciences Centre, Hammersmith Hospital, London W12 0NN, UK. ; Section of Epigenomics and Disease, Department of Medicine, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London W12 0NN, UK. ; Department of Pediatrics and Medicine, Division of Critical Care Medicine and Cardiovascular Pulmonary Research Laboratories, University of Colorado Denver, Denver, Colorado 80045, USA. ; Transgenics and Embryonic Stem Cell Laboratory, Medical Research Council Clinical Sciences Centre, Hammersmith Hospital, London W12 0NN, UK. ; Institute of Molecular Biology and Medicine, 3 Togolok Moldo Street, Bishkek 720040, Kyrgyzstan. ; Section of Cell Biology and Functional Genomics, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, Hammersmith Hospital, London W12 0NN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26258299" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Congenic ; Anoxia/genetics/*metabolism ; Arterioles/metabolism ; Cation Transport Proteins/deficiency/genetics/*metabolism ; Cattle ; Cell Hypoxia ; Cell Proliferation ; Cells, Cultured ; Chromosomes, Mammalian/genetics ; Chronic Disease ; Female ; Gene Knockdown Techniques ; Homeostasis ; Humans ; Hypertension, Pulmonary/genetics/*metabolism ; Intracellular Space/metabolism ; Male ; Muscle, Smooth, Vascular/cytology/*metabolism ; Rats ; Rats, Inbred F344 ; Rats, Inbred WKY ; Zinc/metabolism
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  • 7
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    Mechanistic insights into the recycling machine of the SNARE complex (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-01-13
    Description: Evolutionarily conserved SNARE (soluble N-ethylmaleimide sensitive factor attachment protein receptors) proteins form a complex that drives membrane fusion in eukaryotes. The ATPase NSF (N-ethylmaleimide sensitive factor), together with SNAPs (soluble NSF attachment protein), disassembles the SNARE complex into its protein components, making individual SNAREs available for subsequent rounds of fusion. Here we report structures of ATP- and ADP-bound NSF, and the NSF/SNAP/SNARE (20S) supercomplex determined by single-particle electron cryomicroscopy at near-atomic to sub-nanometre resolution without imposing symmetry. Large, potentially force-generating, conformational differences exist between ATP- and ADP-bound NSF. The 20S supercomplex exhibits broken symmetry, transitioning from six-fold symmetry of the NSF ATPase domains to pseudo four-fold symmetry of the SNARE complex. SNAPs interact with the SNARE complex with an opposite structural twist, suggesting an unwinding mechanism. The interfaces between NSF, SNAPs, and SNAREs exhibit characteristic electrostatic patterns, suggesting how one NSF/SNAP species can act on many different SNARE complexes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4320033/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4320033/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, Minglei -- Wu, Shenping -- Zhou, Qiangjun -- Vivona, Sandro -- Cipriano, Daniel J -- Cheng, Yifan -- Brunger, Axel T -- 5-U01AI082051-05/AI/NIAID NIH HHS/ -- P50 GM082250/GM/NIGMS NIH HHS/ -- P50GM082250/GM/NIGMS NIH HHS/ -- R01 GM082893/GM/NIGMS NIH HHS/ -- R01 GM098672/GM/NIGMS NIH HHS/ -- R01GM082893/GM/NIGMS NIH HHS/ -- R01GM098672/GM/NIGMS NIH HHS/ -- R37 MH063105/MH/NIMH NIH HHS/ -- R37MH63105/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Feb 5;518(7537):61-7. doi: 10.1038/nature14148. Epub 2015 Jan 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA. ; Keck Advanced Microscopy Laboratory, Department of Biochemistry and Biophysics, University of California, San Francisco, California 94158, USA. ; 1] Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA [2] Department of Neurology and Neurological Sciences, Department of Structural Biology, Department of Photon Science, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25581794" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Cricetulus ; Cryoelectron Microscopy ; Models, Molecular ; Multiprotein Complexes/*chemistry/*metabolism/ultrastructure ; N-Ethylmaleimide-Sensitive Proteins/chemistry/metabolism/ultrastructure ; Protein Binding ; Protein Structure, Tertiary ; Rats ; SNARE Proteins/*chemistry/*metabolism/ultrastructure ; Soluble N-Ethylmaleimide-Sensitive Factor Attachment ; Proteins/chemistry/metabolism/ultrastructure
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Business: The billion-dollar biotech (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-06-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dolgin, Elie -- England -- Nature. 2015 Jun 4;522(7554):26-8. doi: 10.1038/522026a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26040878" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology/*economics/trends ; Drug Industry/*economics/trends ; Erythropoietin/biosynthesis/genetics ; Humans ; Massachusetts ; Mice ; Patents as Topic ; Primates ; *RNA, Messenger/administration & dosage/biosynthesis/genetics ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    A temporal shift in the circuits mediating retrieval of fear memory (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-01-21
    Description: Fear memories allow animals to avoid danger, thereby increasing their chances of survival. Fear memories can be retrieved long after learning, but little is known about how retrieval circuits change with time. Here we show that the dorsal midline thalamus of rats is required for the retrieval of auditory conditioned fear at late (24 hours, 7 days, 28 days), but not early (0.5 hours, 6 hours) time points after learning. Consistent with this, the paraventricular nucleus of the thalamus (PVT), a subregion of the dorsal midline thalamus, showed increased c-Fos expression only at late time points, indicating that the PVT is gradually recruited for fear retrieval. Accordingly, the conditioned tone responses of PVT neurons increased with time after training. The prelimbic (PL) prefrontal cortex, which is necessary for fear retrieval, sends dense projections to the PVT. Retrieval at late time points activated PL neurons projecting to the PVT, and optogenetic silencing of these projections impaired retrieval at late, but not early, time points. In contrast, silencing of PL inputs to the basolateral amygdala impaired retrieval at early, but not late, time points, indicating a time-dependent shift in retrieval circuits. Retrieval at late time points also activated PVT neurons projecting to the central nucleus of the amygdala, and silencing these projections at late, but not early, time points induced a persistent attenuation of fear. Thus, the PVT may act as a crucial thalamic node recruited into cortico-amygdalar networks for retrieval and maintenance of long-term fear memories.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376623/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4376623/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Do-Monte, Fabricio H -- Quinones-Laracuente, Kelvin -- Quirk, Gregory J -- G12 MD007600/MD/NIMHD NIH HHS/ -- K99 MH105549/MH/NIMH NIH HHS/ -- P50 MH086400/MH/NIMH NIH HHS/ -- P50-MH086400/MH/NIMH NIH HHS/ -- R01-MH058883/MH/NIMH NIH HHS/ -- R25 GM061838/GM/NIGMS NIH HHS/ -- R25-GM061838/GM/NIGMS NIH HHS/ -- R37 MH058883/MH/NIMH NIH HHS/ -- England -- Nature. 2015 Mar 26;519(7544):460-3. doi: 10.1038/nature14030. Epub 2015 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Psychiatry, University of Puerto Rico School of Medicine, PO Box 365067, San Juan 00936, Puerto Rico [2] Department of Anatomy &Neurobiology, University of Puerto Rico School of Medicine, P.O. Box 365067, San Juan 00936, Puerto Rico.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25600268" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/cytology/physiology ; Animals ; Conditioning (Psychology)/physiology ; Fear/*physiology ; Male ; Memory/*physiology ; Neural Pathways/cytology/*physiology ; Neurons/physiology ; Optogenetics ; Prefrontal Cortex/cytology/physiology ; Proto-Oncogene Proteins c-fos/metabolism ; Rats ; Rats, Sprague-Dawley ; Thalamus/cytology/physiology ; Time Factors
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  • 10
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    Ageing research: Blood to blood (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scudellari, Megan -- England -- Nature. 2015 Jan 22;517(7535):426-9. doi: 10.1038/517426a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25612035" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*blood ; Alzheimer Disease/blood/therapy ; Animals ; Blood Component Removal ; Blood Transfusion ; Bone Morphogenetic Proteins/pharmacology ; Caloric Restriction ; Clinical Trials as Topic ; Female ; Geriatrics/*methods ; Growth Differentiation Factors/pharmacology ; Humans ; Longevity/drug effects ; Male ; Memory/drug effects ; Mice ; Myoblasts, Skeletal/cytology/drug effects ; Neuronal Plasticity/drug effects ; Neurons/cytology/drug effects ; Oxytocin/metabolism/pharmacology ; Plasma/chemistry/physiology ; Rats ; Rejuvenation/*physiology ; Sirolimus/adverse effects/pharmacology
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  • 11
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    Conservation: Giant tortoises hatch on Galapagos island (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-01-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aguilera, Washington Tapia -- Malaga, Jeffreys -- Gibbs, James P -- England -- Nature. 2015 Jan 15;517(7534):271. doi: 10.1038/517271a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Galapagos Conservancy, Santa Cruz, Galapagos, Ecuador. ; Galapagos National Park, San Cristobal, Galapagos, Ecuador. ; State University of New York College of Environmental Science and Forestry, Syracuse, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25592525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Conservation of Natural Resources ; Ecuador ; Population Dynamics ; Rats ; Reproduction/physiology ; Rodent Control ; Turtles/*physiology
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    Grid cell symmetry is shaped by environmental geometry (2015)
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    Publication Date: 2015-02-13
    Description: Grid cells represent an animal's location by firing in multiple fields arranged in a striking hexagonal array. Such an impressive and constant regularity prompted suggestions that grid cells represent a universal and environmental-invariant metric for navigation. Originally the properties of grid patterns were believed to be independent of the shape of the environment and this notion has dominated almost all theoretical grid cell models. However, several studies indicate that environmental boundaries influence grid firing, though the strength, nature and longevity of this effect is unclear. Here we show that grid orientation, scale, symmetry and homogeneity are strongly and permanently affected by environmental geometry. We found that grid patterns orient to the walls of polarized enclosures such as squares, but not circles. Furthermore, the hexagonal grid symmetry is permanently broken in highly polarized environments such as trapezoids, the pattern being more elliptical and less homogeneous. Our results provide compelling evidence for the idea that environmental boundaries compete with the internal organization of the grid cell system to drive grid firing. Notably, grid cell activity is more local than previously thought and as a consequence cannot provide a universal spatial metric in all environments.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4576734/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4576734/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krupic, Julija -- Bauza, Marius -- Burton, Stephen -- Barry, Caswell -- O'Keefe, John -- 101590/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2015 Feb 12;518(7538):232-5. doi: 10.1038/nature14153.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK. ; 1] Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK [2] Sainsbury Wellcome Centre, University College London, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25673417" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Entorhinal Cortex/*cytology/physiology ; *Environment ; Male ; Models, Neurological ; Neurons/*cytology/physiology ; Orientation/*physiology ; Pattern Recognition, Visual/physiology ; Rats ; Rotation ; Space Perception/*physiology
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    Repeated ER-endosome contacts promote endosome translocation and neurite outgrowth (2015)
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    Publication Date: 2015-04-10
    Description: The main organelles of the secretory and endocytic pathways--the endoplasmic reticulum (ER) and endosomes, respectively--are connected through contact sites whose numbers increase as endosomes mature. One function of such sites is to enable dephosphorylation of the cytosolic tails of endosomal signalling receptors by an ER-associated phosphatase, whereas others serve to negatively control the association of endosomes with the minus-end-directed microtubule motor dynein or mediate endosome fission. Cholesterol transfer and Ca(2+) exchange have been proposed as additional functions of such sites. However, the compositions, activities and regulations of ER-endosome contact sites remain incompletely understood. Here we show in human and rat cell lines that protrudin, an ER protein that promotes protrusion and neurite outgrowth, forms contact sites with late endosomes (LEs) via coincident detection of the small GTPase RAB7 and phosphatidylinositol 3-phosphate (PtdIns(3)P). These contact sites mediate transfer of the microtubule motor kinesin 1 from protrudin to the motor adaptor FYCO1 on LEs. Repeated LE-ER contacts promote microtubule-dependent translocation of LEs to the cell periphery and subsequent synaptotagmin-VII-dependent fusion with the plasma membrane. Such fusion induces outgrowth of protrusions and neurites, which requires the abilities of protrudin and FYCO1 to interact with LEs and kinesin 1. Thus, protrudin-containing ER-LE contact sites are platforms for kinesin-1 loading onto LEs, and kinesin-1-mediated translocation of LEs to the plasma membrane, fuelled by repeated ER contacts, promotes protrusion and neurite outgrowth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raiborg, Camilla -- Wenzel, Eva M -- Pedersen, Nina M -- Olsvik, Hallvard -- Schink, Kay O -- Schultz, Sebastian W -- Vietri, Marina -- Nisi, Veronica -- Bucci, Cecilia -- Brech, Andreas -- Johansen, Terje -- Stenmark, Harald -- England -- Nature. 2015 Apr 9;520(7546):234-8. doi: 10.1038/nature14359.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Montebello, N-0379 Oslo, Norway [2] Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, Montebello, N-0379 Oslo, Norway. ; Institute of Medical Biology, University of Tromso - The Arctic University of Norway, N-9037 Tromso, Norway. ; Department of Biological and Environmental Sciences and Technologies (DiSTeBA), University of Salento, Via Provinciale Monteroni 165, 73100 Lecce, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25855459" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Biological Transport ; Cell Line ; Cell Membrane/metabolism ; DNA-Binding Proteins/metabolism ; Endoplasmic Reticulum/*metabolism ; Endosomes/*metabolism ; HeLa Cells ; Humans ; Kinesin/metabolism ; Microtubules/metabolism ; Neurites/*metabolism ; Phosphatidylinositol Phosphates/metabolism ; Rats ; Synaptotagmins/metabolism ; Transcription Factors/metabolism ; Vesicular Transport Proteins/metabolism ; rab GTP-Binding Proteins/metabolism
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    Gating machinery of InsP3R channels revealed by electron cryomicroscopy (2015)
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    Publication Date: 2015-10-13
    Description: Inositol-1,4,5-trisphosphate receptors (InsP3Rs) are ubiquitous ion channels responsible for cytosolic Ca(2+) signalling and essential for a broad array of cellular processes ranging from contraction to secretion, and from proliferation to cell death. Despite decades of research on InsP3Rs, a mechanistic understanding of their structure-function relationship is lacking. Here we present the first, to our knowledge, near-atomic (4.7 A) resolution electron cryomicroscopy structure of the tetrameric mammalian type 1 InsP3R channel in its apo-state. At this resolution, we are able to trace unambiguously approximately 85% of the protein backbone, allowing us to identify the structural elements involved in gating and modulation of this 1.3-megadalton channel. Although the central Ca(2+)-conduction pathway is similar to other ion channels, including the closely related ryanodine receptor, the cytosolic carboxy termini are uniquely arranged in a left-handed alpha-helical bundle, directly interacting with the amino-terminal domains of adjacent subunits. This configuration suggests a molecular mechanism for allosteric regulation of channel gating by intracellular signals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fan, Guizhen -- Baker, Matthew L -- Wang, Zhao -- Baker, Mariah R -- Sinyagovskiy, Pavel A -- Chiu, Wah -- Ludtke, Steven J -- Serysheva, Irina I -- P41 GM103832/GM/NIGMS NIH HHS/ -- P41GM103832/GM/NIGMS NIH HHS/ -- R01 GM072804/GM/NIGMS NIH HHS/ -- R01 GM079429/GM/NIGMS NIH HHS/ -- R01 GM080139/GM/NIGMS NIH HHS/ -- R01GM072804/GM/NIGMS NIH HHS/ -- R01GM079429/GM/NIGMS NIH HHS/ -- R01GM080139/GM/NIGMS NIH HHS/ -- R21 AR063255/AR/NIAMS NIH HHS/ -- R21 GM100229/GM/NIGMS NIH HHS/ -- R21AR063255/AR/NIAMS NIH HHS/ -- R21GM100229/GM/NIGMS NIH HHS/ -- S10 OD016279/OD/NIH HHS/ -- S10OD016279/OD/NIH HHS/ -- England -- Nature. 2015 Nov 19;527(7578):336-41. doi: 10.1038/nature15249. Epub 2015 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Structural Biology Imaging Center, The University of Texas Medical School at Houston, 6431 Fannin Street, Houston, Texas 77030, USA. ; National Center for Macromolecular Imaging, Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26458101" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Animals ; Apoproteins/chemistry/metabolism/ultrastructure ; Calcium/metabolism ; Calcium Signaling ; *Cryoelectron Microscopy ; Cytosol/chemistry/metabolism ; Inositol 1,4,5-Trisphosphate Receptors/chemistry/*metabolism/*ultrastructure ; Ion Channel Gating ; Models, Molecular ; Protein Folding ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein Subunits/chemistry/metabolism ; Rats ; Ryanodine Receptor Calcium Release Channel/chemistry/metabolism
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    Genetics: No more addictive personality (2015)
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    Publication Date: 2015-06-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Szalavitz, Maia -- England -- Nature. 2015 Jun 25;522(7557):S48-9. doi: 10.1038/522S48a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26107094" target="_blank"〉PubMed〈/a〉
    Keywords: Alcoholism/complications/genetics ; Aldehyde Dehydrogenase/genetics ; Animals ; Antisocial Personality Disorder/complications/genetics ; Anxiety/complications/genetics ; Behavior, Addictive/enzymology/*genetics/metabolism/*psychology ; Cocaine/administration & dosage/adverse effects ; Epigenesis, Genetic/genetics ; Humans ; Metabolism/genetics ; Methyl-CpG-Binding Protein 2/genetics ; Mice ; Nerve Tissue Proteins/genetics ; Personality ; *Precision Medicine/trends ; Rats ; Receptors, Nicotinic/genetics ; Serotonin Plasma Membrane Transport Proteins/genetics/metabolism ; Stress Disorders, Traumatic/genetics/psychology ; Substance-Related Disorders/complications/genetics ; Temperament ; Tobacco Use Disorder/genetics
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    'Organs-on-chips' go mainstream (2015)
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    Publication Date: 2015-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reardon, Sara -- England -- Nature. 2015 Jul 16;523(7560):266. doi: 10.1038/523266a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26178942" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotechnology/methods ; Clinical Trials as Topic ; Drug Discovery/*methods ; Drug Industry/*methods ; Humans ; *Models, Biological ; Organ Specificity/*drug effects ; Rats ; Reproducibility of Results ; Tissue Array Analysis/*methods
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    Pharmacotherapy: Quest for the quitting pill (2015)
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    Publication Date: 2015-06-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willyard, Cassandra -- England -- Nature. 2015 Jun 25;522(7557):S53-5. doi: 10.1038/522S53a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26107096" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Addictive/*drug therapy/immunology/*psychology ; Buprenorphine/therapeutic use ; Buprenorphine, Naloxone Drug Combination ; Clinical Trials as Topic ; Cocaine-Related Disorders/drug therapy/immunology/psychology ; Counseling ; Dopamine/metabolism ; *Drug Discovery/economics ; Drug Industry/economics ; Humans ; Ibogaine/analogs & derivatives/pharmacology/therapeutic use ; Lobeline/therapeutic use ; Molecular Targeted Therapy ; Naloxone/therapeutic use ; Naltrexone/therapeutic use ; Oligopeptides/pharmacology/therapeutic use ; Opioid-Related Disorders/drug therapy/immunology/psychology ; Pleasure/*drug effects/physiology ; Rats ; Receptors, Nicotinic/metabolism ; *Reward ; Substance-Related Disorders/*drug therapy/immunology/*psychology ; Tobacco Use Disorder/drug therapy/immunology ; Vaccines/administration & dosage/immunology/therapeutic use ; Vesicular Monoamine Transport Proteins/metabolism
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    Epicardial FSTL1 reconstitution regenerates the adult mammalian heart (2015)
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    Publication Date: 2015-09-17
    Description: The elucidation of factors that activate the regeneration of the adult mammalian heart is of major scientific and therapeutic importance. Here we found that epicardial cells contain a potent cardiogenic activity identified as follistatin-like 1 (Fstl1). Epicardial Fstl1 declines following myocardial infarction and is replaced by myocardial expression. Myocardial Fstl1 does not promote regeneration, either basally or upon transgenic overexpression. Application of the human Fstl1 protein (FSTL1) via an epicardial patch stimulates cell cycle entry and division of pre-existing cardiomyocytes, improving cardiac function and survival in mouse and swine models of myocardial infarction. The data suggest that the loss of epicardial FSTL1 is a maladaptive response to injury, and that its restoration would be an effective way to reverse myocardial death and remodelling following myocardial infarction in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762253/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4762253/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wei, Ke -- Serpooshan, Vahid -- Hurtado, Cecilia -- Diez-Cunado, Marta -- Zhao, Mingming -- Maruyama, Sonomi -- Zhu, Wenhong -- Fajardo, Giovanni -- Noseda, Michela -- Nakamura, Kazuto -- Tian, Xueying -- Liu, Qiaozhen -- Wang, Andrew -- Matsuura, Yuka -- Bushway, Paul -- Cai, Wenqing -- Savchenko, Alex -- Mahmoudi, Morteza -- Schneider, Michael D -- van den Hoff, Maurice J B -- Butte, Manish J -- Yang, Phillip C -- Walsh, Kenneth -- Zhou, Bin -- Bernstein, Daniel -- Mercola, Mark -- Ruiz-Lozano, Pilar -- 5UM1 HL113456/HL/NHLBI NIH HHS/ -- HL065484/HL/NHLBI NIH HHS/ -- HL108176/HL/NHLBI NIH HHS/ -- HL113601/HL/NHLBI NIH HHS/ -- HL116591/HL/NHLBI NIH HHS/ -- K08 AI079268/AI/NIAID NIH HHS/ -- P01 HL098053/HL/NHLBI NIH HHS/ -- P30 AR061303/AR/NIAMS NIH HHS/ -- P30 CA030199/CA/NCI NIH HHS/ -- R01 HL086879/HL/NHLBI NIH HHS/ -- R01 HL113601/HL/NHLBI NIH HHS/ -- UM1 HL113456/HL/NHLBI NIH HHS/ -- England -- Nature. 2015 Sep 24;525(7570):479-85. doi: 10.1038/nature15372. Epub 2015 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, University of California, San Diego, La Jolla, California 92037, USA. ; Sanford-Burnham-Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, California 92037, USA. ; Stanford Cardiovascular Institute and Department of Pediatrics, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA. ; Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts 02118, USA. ; Imperial College London, Faculty of Medicine, Imperial Centre for Translational and Experimental Medicine, Du Cane Road, London W12 0NN, UK. ; Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, and Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China. ; Nanotechnology Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, 1417613151 Tehran, Iran. ; Academic Medical Center. Dept Anatomy, Embryology and Physiology. Meibergdreef 15. 1105AZ Amsterdam, The Netherlands. ; CAS Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26375005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/drug effects ; Cell Proliferation/drug effects ; Culture Media, Conditioned/pharmacology ; Female ; Follistatin-Related Proteins/genetics/*metabolism ; Humans ; Male ; Mice ; Myoblasts, Cardiac/cytology/drug effects ; Myocardial Infarction/genetics/metabolism/pathology/physiopathology ; Myocardium/*metabolism ; Myocytes, Cardiac/cytology/drug effects/metabolism ; Pericardium/cytology/drug effects/*growth & development/*metabolism ; Rats ; *Regeneration/drug effects ; Signal Transduction ; Swine ; Transgenes/genetics
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    Microbiology: Inflammatory evidence (2015)
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    Publication Date: 2015-12-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weir, Kirsten -- England -- Nature. 2015 Dec 17;528(7582):S130-1. doi: 10.1038/528S130a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26672786" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Chronic Disease/prevention & control/therapy ; DNA Damage ; Growth Differentiation Factor 15/metabolism ; Humans ; Inflammation/*complications/microbiology/pathology/therapy ; Male ; Mice ; Oxidative Stress ; Prostatic Neoplasms/*etiology/microbiology/*pathology/prevention & control ; Prostatitis/*complications/microbiology/pathology/therapy ; Rats
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    Ultrafast ultrasound localization microscopy for deep super-resolution vascular imaging (2015)
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    Publication Date: 2015-11-27
    Description: Non-invasive imaging deep into organs at microscopic scales remains an open quest in biomedical imaging. Although optical microscopy is still limited to surface imaging owing to optical wave diffusion and fast decorrelation in tissue, revolutionary approaches such as fluorescence photo-activated localization microscopy led to a striking increase in resolution by more than an order of magnitude in the last decade. In contrast with optics, ultrasonic waves propagate deep into organs without losing their coherence and are much less affected by in vivo decorrelation processes. However, their resolution is impeded by the fundamental limits of diffraction, which impose a long-standing trade-off between resolution and penetration. This limits clinical and preclinical ultrasound imaging to a sub-millimetre scale. Here we demonstrate in vivo that ultrasound imaging at ultrafast frame rates (more than 500 frames per second) provides an analogue to optical localization microscopy by capturing the transient signal decorrelation of contrast agents--inert gas microbubbles. Ultrafast ultrasound localization microscopy allowed both non-invasive sub-wavelength structural imaging and haemodynamic quantification of rodent cerebral microvessels (less than ten micrometres in diameter) more than ten millimetres below the tissue surface, leading to transcranial whole-brain imaging within short acquisition times (tens of seconds). After intravenous injection, single echoes from individual microbubbles were detected through ultrafast imaging. Their localization, not limited by diffraction, was accumulated over 75,000 images, yielding 1,000,000 events per coronal plane and statistically independent pixels of ten micrometres in size. Precise temporal tracking of microbubble positions allowed us to extract accurately in-plane velocities of the blood flow with a large dynamic range (from one millimetre per second to several centimetres per second). These results pave the way for deep non-invasive microscopy in animals and humans using ultrasound. We anticipate that ultrafast ultrasound localization microscopy may become an invaluable tool for the fundamental understanding and diagnostics of various disease processes that modify the microvascular blood flow, such as cancer, stroke and arteriosclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Errico, Claudia -- Pierre, Juliette -- Pezet, Sophie -- Desailly, Yann -- Lenkei, Zsolt -- Couture, Olivier -- Tanter, Mickael -- England -- Nature. 2015 Nov 26;527(7579):499-502. doi: 10.1038/nature16066.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM, Institut Langevin, 1 rue Jussieu, 75005 Paris, France. ; Institut Langevin, ESPCI-ParisTech, PSL Research University, 1 rue Jussieu, 75005 Paris, France. ; CNRS UMR 7587, 1 rue Jussieu, 75005 Paris, France. ; CNRS, UMR 8249, 10 rue Vauquelin, 75005 Paris, France. ; Brain Plasticity Unit, ESPCI-ParisTech, PSL Research University, 10 rue Vauquelin, 75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26607546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*blood supply/cytology ; Contrast Media ; Male ; Microbubbles ; Microscopy/*methods ; *Microvessels ; Molecular Imaging/*methods ; Optics and Photonics ; Rats ; Rats, Sprague-Dawley ; Time Factors ; Ultrasonics/*methods
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    Shearing-induced asymmetry in entorhinal grid cells (2015)
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    Publication Date: 2015-02-13
    Description: Grid cells are neurons with periodic spatial receptive fields (grids) that tile two-dimensional space in a hexagonal pattern. To provide useful information about location, grids must be stably anchored to an external reference frame. The mechanisms underlying this anchoring process have remained elusive. Here we show in differently sized familiar square enclosures that the axes of the grids are offset from the walls by an angle that minimizes symmetry with the borders of the environment. This rotational offset is invariably accompanied by an elliptic distortion of the grid pattern. Reversing the ellipticity analytically by a shearing transformation removes the angular offset. This, together with the near-absence of rotation in novel environments, suggests that the rotation emerges through non-coaxial strain as a function of experience. The systematic relationship between rotation and distortion of the grid pattern points to shear forces arising from anchoring to specific geometric reference points as key elements of the mechanism for alignment of grid patterns to the external world.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stensola, Tor -- Stensola, Hanne -- Moser, May-Britt -- Moser, Edvard I -- England -- Nature. 2015 Feb 12;518(7538):207-12. doi: 10.1038/nature14151.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kavli Institute for Systems Neuroscience and Centre for Neural Computation, Norwegian University of Science and Technology, Olav Kyrres gate 9, 7491 Trondheim, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25673414" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain Mapping ; Entorhinal Cortex/*cytology/physiology ; *Environment ; Male ; Models, Neurological ; Neurons/cytology/*physiology ; Orientation/*physiology ; Pattern Recognition, Visual/*physiology ; Rats ; Rats, Long-Evans ; Rotation ; Space Perception/*physiology ; Time Factors
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    Nanoparticle biointerfacing by platelet membrane cloaking (2015)
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    Publication Date: 2015-09-17
    Description: Development of functional nanoparticles can be encumbered by unanticipated material properties and biological events, which can affect nanoparticle effectiveness in complex, physiologically relevant systems. Despite the advances in bottom-up nanoengineering and surface chemistry, reductionist functionalization approaches remain inadequate in replicating the complex interfaces present in nature and cannot avoid exposure of foreign materials. Here we report on the preparation of polymeric nanoparticles enclosed in the plasma membrane of human platelets, which are a unique population of cellular fragments that adhere to a variety of disease-relevant substrates. The resulting nanoparticles possess a right-side-out unilamellar membrane coating functionalized with immunomodulatory and adhesion antigens associated with platelets. Compared to uncoated particles, the platelet membrane-cloaked nanoparticles have reduced cellular uptake by macrophage-like cells and lack particle-induced complement activation in autologous human plasma. The cloaked nanoparticles also display platelet-mimicking properties such as selective adhesion to damaged human and rodent vasculatures as well as enhanced binding to platelet-adhering pathogens. In an experimental rat model of coronary restenosis and a mouse model of systemic bacterial infection, docetaxel and vancomycin, respectively, show enhanced therapeutic efficacy when delivered by the platelet-mimetic nanoparticles. The multifaceted biointerfacing enabled by the platelet membrane cloaking method provides a new approach in developing functional nanoparticles for disease-targeted delivery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Che-Ming J -- Fang, Ronnie H -- Wang, Kuei-Chun -- Luk, Brian T -- Thamphiwatana, Soracha -- Dehaini, Diana -- Nguyen, Phu -- Angsantikul, Pavimol -- Wen, Cindy H -- Kroll, Ashley V -- Carpenter, Cody -- Ramesh, Manikantan -- Qu, Vivian -- Patel, Sherrina H -- Zhu, Jie -- Shi, William -- Hofman, Florence M -- Chen, Thomas C -- Gao, Weiwei -- Zhang, Kang -- Chien, Shu -- Zhang, Liangfang -- R01DK095168/DK/NIDDK NIH HHS/ -- R01EY25090/EY/NEI NIH HHS/ -- R01HL108735/HL/NHLBI NIH HHS/ -- R25CA153915/CA/NCI NIH HHS/ -- England -- Nature. 2015 Oct 1;526(7571):118-21. doi: 10.1038/nature15373. Epub 2015 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of NanoEngineering, University of California, San Diego, La Jolla, California 92093, USA. ; Moores Cancer Center, University of California, San Diego, La Jolla, California 92093, USA. ; Department of Bioengineering, University of California, San Diego, La Jolla, California 92093, USA. ; Institute of Engineering in Medicine, University of California, San Diego, La Jolla, California 92093, USA. ; Shiley Eye Institute, University of California, San Diego, La Jolla, California 92093, USA. ; Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA. ; Veterans Administration Healthcare System, San Diego, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26374997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/*administration & dosage/pharmacokinetics ; Blood Platelets/*cytology ; Blood Vessels/cytology/metabolism/pathology ; Cell Membrane/*metabolism ; Collagen/chemistry/immunology ; Complement Activation/immunology ; Coronary Restenosis/blood/drug therapy/metabolism ; Disease Models, Animal ; Drug Delivery Systems/*methods ; Humans ; Macrophages/immunology ; Male ; Mice ; Nanoparticles/*administration & dosage/*chemistry ; *Platelet Adhesiveness ; Polymers/chemistry ; Rats ; Rats, Sprague-Dawley ; Staphylococcal Infections/blood/drug therapy/metabolism/microbiology ; Staphylococcus aureus/cytology/metabolism ; Taxoids/administration & dosage/pharmacokinetics ; Unilamellar Liposomes/chemistry ; Vancomycin/administration & dosage/pharmacokinetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Addiction: 4 big questions (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-06-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holmes, David -- England -- Nature. 2015 Jun 25;522(7557):S63. doi: 10.1038/522S63a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26107101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive/classification/genetics/physiopathology/prevention & ; control/rehabilitation ; Brain/drug effects/physiology/physiopathology ; Dopamine Antagonists/pharmacology/therapeutic use ; Gene-Environment Interaction ; Genetic Predisposition to Disease/genetics ; Humans ; Mice ; Molecular Targeted Therapy ; Optogenetics ; Rats ; Receptors, Dopamine/metabolism ; Reward ; Secondary Prevention/methods ; *Substance-Related Disorders/classification/genetics/physiopathology/prevention & ; control/rehabilitation ; Vaccines/economics/therapeutic use
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Neuroscience: Rewiring the brain (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-06-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bourzac, Katherine -- England -- Nature. 2015 Jun 25;522(7557):S50-2. doi: 10.1038/522S50a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26107095" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aging/physiology ; Alcoholism/physiopathology/psychology/rehabilitation ; Animals ; Behavior, Addictive/*physiopathology/psychology/rehabilitation ; Brain/*physiology/*physiopathology ; Child ; Disease Models, Animal ; Humans ; *Neural Pathways ; Rats
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Distinct relationships of parietal and prefrontal cortices to evidence accumulation (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-01-21
    Description: Gradual accumulation of evidence is thought to be fundamental for decision-making, and its neural correlates have been found in several brain regions. Here we develop a generalizable method to measure tuning curves that specify the relationship between neural responses and mentally accumulated evidence, and apply it to distinguish the encoding of decision variables in posterior parietal cortex and prefrontal cortex (frontal orienting fields, FOF). We recorded the firing rates of neurons in posterior parietal cortex and FOF from rats performing a perceptual decision-making task. Classical analyses uncovered correlates of accumulating evidence, similar to previous observations in primates and also similar across the two regions. However, tuning curve assays revealed that while the posterior parietal cortex encodes a graded value of the accumulating evidence, the FOF has a more categorical encoding that indicates, throughout the trial, the decision provisionally favoured by the evidence accumulated so far. Contrary to current views, this suggests that premotor activity in the frontal cortex does not have a role in the accumulation process, but instead has a more categorical function, such as transforming accumulated evidence into a discrete choice. To probe causally the role of FOF activity, we optogenetically silenced it during different time points of the trial. Consistent with a role in committing to a categorical choice at the end of the evidence accumulation process, but not consistent with a role during the accumulation itself, a behavioural effect was observed only when FOF silencing occurred at the end of the perceptual stimulus. Our results place important constraints on the circuit logic of brain regions involved in decision-making.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanks, Timothy D -- Kopec, Charles D -- Brunton, Bingni W -- Duan, Chunyu A -- Erlich, Jeffrey C -- Brody, Carlos D -- F32 MH098572/MH/NIMH NIH HHS/ -- F32MH098572/MH/NIMH NIH HHS/ -- T32MH065214/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Apr 9;520(7546):220-3. doi: 10.1038/nature14066. Epub 2015 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Princeton Neuroscience Institute, Princeton University, Princeton, New Jersey 08544, USA [2] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA. ; 1] Princeton Neuroscience Institute, Princeton University, Princeton, New Jersey 08544, USA [2] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA [3] Departments of Biology and Applied Mathematics, University of Washington, Seattle, Washington 98105, USA. ; 1] Princeton Neuroscience Institute, Princeton University, Princeton, New Jersey 08544, USA [2] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA [3] NYU-ECNU Institute of Brain and Cognitive Science, NYU-Shanghai, Shanghai 200122, China. ; 1] Princeton Neuroscience Institute, Princeton University, Princeton, New Jersey 08544, USA [2] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA [3] Howard Hughes Medical Institute, Princeton University, Princeton, New Jersey 08544, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25600270" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Decision Making/*physiology ; Halorhodopsins/metabolism ; Male ; Neural Pathways ; Neurons/physiology ; Parietal Lobe/cytology/*physiology ; Prefrontal Cortex/cytology/*physiology ; Rats ; Rats, Long-Evans
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    Evolutionary genomics. Evolutionary changes in promoter and enhancer activity during human corticogenesis (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-03-07
    Description: Human higher cognition is attributed to the evolutionary expansion and elaboration of the human cerebral cortex. However, the genetic mechanisms contributing to these developmental changes are poorly understood. We used comparative epigenetic profiling of human, rhesus macaque, and mouse corticogenesis to identify promoters and enhancers that have gained activity in humans. These gains are significantly enriched in modules of coexpressed genes in the cortex that function in neuronal proliferation, migration, and cortical-map organization. Gain-enriched modules also showed correlated gene expression patterns and similar transcription factor binding site enrichments in promoters and enhancers, suggesting that they are connected by common regulatory mechanisms. Our results reveal coordinated patterns of potential regulatory changes associated with conserved developmental processes during corticogenesis, providing insight into human cortical evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4426903/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4426903/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reilly, Steven K -- Yin, Jun -- Ayoub, Albert E -- Emera, Deena -- Leng, Jing -- Cotney, Justin -- Sarro, Richard -- Rakic, Pasko -- Noonan, James P -- 099175/Z/12/Z/Wellcome Trust/United Kingdom -- DA023999/DA/NIDA NIH HHS/ -- F32 GM106628/GM/NIGMS NIH HHS/ -- GM094780/GM/NIGMS NIH HHS/ -- NS014841/NS/NINDS NIH HHS/ -- P30 CA016359/CA/NCI NIH HHS/ -- R01 DA023999/DA/NIDA NIH HHS/ -- R01 GM094780/GM/NIGMS NIH HHS/ -- T32 GM007223/GM/NIGMS NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2015 Mar 6;347(6226):1155-9. doi: 10.1126/science.1260943.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Yale School of Medicine, New Haven, CT 06510, USA. ; Kavli Institute for Neuroscience, Yale School of Medicine, New Haven, CT 06510, USA. Department of Neurobiology, Yale School of Medicine, New Haven, CT 06510, USA. ; Department of Genetics, Yale School of Medicine, New Haven, CT 06510, USA. Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06511, USA. ; Department of Genetics, Yale School of Medicine, New Haven, CT 06510, USA. Kavli Institute for Neuroscience, Yale School of Medicine, New Haven, CT 06510, USA. Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT 06511, USA. james.noonan@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25745175" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/*growth & development ; Enhancer Elements, Genetic/*genetics ; *Epigenesis, Genetic ; *Evolution, Molecular ; *Gene Expression Regulation, Developmental ; Humans ; Macaca mulatta ; Mice ; Organogenesis/*genetics ; Promoter Regions, Genetic/*genetics ; Rats
    Print ISSN: 0036-8075
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    Brain crystals (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-10-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krupic, Julija -- New York, N.Y. -- Science. 2015 Oct 2;350(6256):47. doi: 10.1126/science.aad3002.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK. j.krupic@ucl.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26430112" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; Brain/*physiology/*ultrastructure ; *Distance Perception ; Fourier Analysis ; Humans ; Metric System ; Neurons/*physiology/*ultrastructure ; Rats ; Spatial Navigation/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    NEUROSCIENCE. Virtual rat brain fails to impress its critics (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-10-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kupferschmidt, Kai -- New York, N.Y. -- Science. 2015 Oct 16;350(6258):263-4. doi: 10.1126/science.350.6258.263.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26472886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/*ultrastructure ; *Computer Simulation ; Investments ; *Models, Neurological ; Neurons/*ultrastructure ; Neurosciences/*economics ; Rats
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Axonal regeneration. Systemic administration of epothilone B promotes axon regeneration after spinal cord injury (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-03-15
    Description: After central nervous system (CNS) injury, inhibitory factors in the lesion scar and poor axon growth potential prevent axon regeneration. Microtubule stabilization reduces scarring and promotes axon growth. However, the cellular mechanisms of this dual effect remain unclear. Here, delayed systemic administration of a blood-brain barrier-permeable microtubule-stabilizing drug, epothilone B (epoB), decreased scarring after rodent spinal cord injury (SCI) by abrogating polarization and directed migration of scar-forming fibroblasts. Conversely, epothilone B reactivated neuronal polarization by inducing concerted microtubule polymerization into the axon tip, which propelled axon growth through an inhibitory environment. Together, these drug-elicited effects promoted axon regeneration and improved motor function after SCI. With recent clinical approval, epothilones hold promise for clinical use after CNS injury.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445125/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445125/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruschel, Jorg -- Hellal, Farida -- Flynn, Kevin C -- Dupraz, Sebastian -- Elliott, David A -- Tedeschi, Andrea -- Bates, Margaret -- Sliwinski, Christopher -- Brook, Gary -- Dobrindt, Kristina -- Peitz, Michael -- Brustle, Oliver -- Norenberg, Michael D -- Blesch, Armin -- Weidner, Norbert -- Bunge, Mary Bartlett -- Bixby, John L -- Bradke, Frank -- R01 HD057632/HD/NICHD NIH HHS/ -- R01 NS059866/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2015 Apr 17;348(6232):347-52. doi: 10.1126/science.aaa2958. Epub 2015 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Axonal Growth and Regeneration, German Center for Neurodegenerative Diseases, Ludwig-Erhard-Allee 2, 53175 Bonn, Germany. ; The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, 1095 Northwest 14th Terrace, Miami, FL33136, USA. ; Spinal Cord Injury Center, Heidelberg University Hospital, Schlierbacher Landstr. 200A, 69118 Heidelberg, Germany. ; Institute for Neuropathology, RWTH Aachen University, Steinbergweg 20, 52074, Aachen, Germany. Julich-Aachen Research Alliance-Translational Brain Medicine. ; Institute of Reconstructive Neurobiology, Life&Brain Center, University of Bonn and Hertie Foundation, Sigmund-Freud-Strasse 25, 53127 Bonn, Germany. ; Departments of Pathology, Biochemistry and Molecular Biology, University of Miami School of Medicine, Miami, FL 33101, USA. ; Axonal Growth and Regeneration, German Center for Neurodegenerative Diseases, Ludwig-Erhard-Allee 2, 53175 Bonn, Germany. frank.bradke@dzne.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25765066" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*drug effects/physiology ; Cell Movement/drug effects ; Cell Polarity/drug effects ; Cicatrix/pathology/*prevention & control ; Epothilones/*administration & dosage ; Fibroblasts/drug effects/pathology ; Humans ; Meninges/drug effects/pathology ; Motor Activity/drug effects ; Nerve Regeneration/*drug effects ; Neurons/drug effects/pathology ; Rats ; Spinal Cord Injuries/*drug therapy/pathology/physiopathology ; Tubulin Modulators/*administration & dosage
    Print ISSN: 0036-8075
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    Spring-loaded unraveling of a single SNARE complex by NSF in one round of ATP turnover (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-03-31
    Description: During intracellular membrane trafficking, N-ethylmaleimide-sensitive factor (NSF) and alpha-soluble NSF attachment protein (alpha-SNAP) disassemble the soluble NSF attachment protein receptor (SNARE) complex for recycling of the SNARE proteins. The molecular mechanism by which NSF disassembles the SNARE complex is largely unknown. Using single-molecule fluorescence spectroscopy and magnetic tweezers, we found that NSF disassembled a single SNARE complex in only one round of adenosine triphosphate (ATP) turnover. Upon ATP cleavage, the NSF hexamer developed internal tension with dissociation of phosphate ions. After latent time measuring tens of seconds, NSF released the built-up tension in a burst within 20 milliseconds, resulting in disassembly followed by immediate release of the SNARE proteins. Thus, NSF appears to use a "spring-loaded" mechanism to couple ATP hydrolysis and unfolding of substrate proteins.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441202/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441202/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ryu, Je-Kyung -- Min, Duyoung -- Rah, Sang-Hyun -- Kim, Soo Jin -- Park, Yongsoo -- Kim, Haesoo -- Hyeon, Changbong -- Kim, Ho Min -- Jahn, Reinhard -- Yoon, Tae-Young -- 3P01GM072694-05S1/GM/NIGMS NIH HHS/ -- P01 GM072694/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Mar 27;347(6229):1485-9. doi: 10.1126/science.aaa5267.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Creative Research Initiative Center for Single-Molecule Systems Biology, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 305-701, South Korea. Department of Physics, KAIST, Daejeon 305-701, South Korea. ; Graduate School of Medical Science and Engineering, KAIST, Daejeon 305-701, South Korea. ; Department of Neurobiology, Max-Planck-Institute for Biophysical Chemistry, 37077 Gottingen, Germany. ; Korea Institute for Advanced Study, Seoul 130-722, South Korea. ; Department of Neurobiology, Max-Planck-Institute for Biophysical Chemistry, 37077 Gottingen, Germany. rjahn@gwdg.de tyyoon@kaist.ac.kr. ; National Creative Research Initiative Center for Single-Molecule Systems Biology, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 305-701, South Korea. Department of Physics, KAIST, Daejeon 305-701, South Korea. rjahn@gwdg.de tyyoon@kaist.ac.kr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25814585" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Cattle ; Cricetinae ; Fluorescence Resonance Energy Transfer ; Hydrolysis ; N-Ethylmaleimide-Sensitive Proteins/*metabolism ; Rats ; SNARE Proteins/*metabolism ; Soluble N-Ethylmaleimide-Sensitive Factor Attachment Proteins/*metabolism ; Spectrometry, Fluorescence
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    ACTIN-DIRECTED TOXIN. ACD toxin-produced actin oligomers poison formin-controlled actin polymerization (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-08-01
    Description: The actin cross-linking domain (ACD) is an actin-specific toxin produced by several pathogens, including life-threatening spp. of Vibrio cholerae, Vibrio vulnificus, and Aeromonas hydrophila. Actin cross-linking by ACD is thought to lead to slow cytoskeleton failure owing to a gradual sequestration of actin in the form of nonfunctional oligomers. Here, we found that ACD converted cytoplasmic actin into highly toxic oligomers that potently "poisoned" the ability of major actin assembly proteins, formins, to sustain actin polymerization. Thus, ACD can target the most abundant cellular protein by using actin oligomers as secondary toxins to efficiently subvert cellular functions of actin while functioning at very low doses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4648357/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4648357/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heisler, David B -- Kudryashova, Elena -- Grinevich, Dmitry O -- Suarez, Cristian -- Winkelman, Jonathan D -- Birukov, Konstantin G -- Kotha, Sainath R -- Parinandi, Narasimham L -- Vavylonis, Dimitrios -- Kovar, David R -- Kudryashov, Dmitri S -- R01 GM079265/GM/NIGMS NIH HHS/ -- R01 GM098430/GM/NIGMS NIH HHS/ -- R01 GM114666/GM/NIGMS NIH HHS/ -- R01 HL076259/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2015 Jul 31;349(6247):535-9. doi: 10.1126/science.aab4090.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, The Ohio State University, Columbus, OH 43210, USA. The Ohio State Biochemistry Program, The Ohio State University, Columbus, OH 43210, USA. ; Department of Chemistry and Biochemistry, The Ohio State University, Columbus, OH 43210, USA. kudryashov.1@osu.edu kudryashova.1@osu.edu. ; Department of Chemistry and Biochemistry, The Ohio State University, Columbus, OH 43210, USA. ; Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA. ; Section of Pulmonary and Critical Care and Lung Injury Center, Department of Medicine, The University of Chicago, Chicago, IL 60637, USA. ; Lipid Signaling and Lipidomics Laboratory, Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine, Dorothy M. Davis Heart and Lung Research Institute, College of Medicine, The Ohio State University, Columbus, OH 43210, USA. ; Department of Physics, Lehigh University, Bethlehem, PA 18015, USA. ; Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA. Department of Biochemistry and Molecular Biology, The University of Chicago, Chicago, IL 60637, USA. ; Department of Chemistry and Biochemistry, The Ohio State University, Columbus, OH 43210, USA. The Ohio State Biochemistry Program, The Ohio State University, Columbus, OH 43210, USA. kudryashov.1@osu.edu kudryashova.1@osu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26228148" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*metabolism ; Animals ; Antigens, Bacterial/*chemistry/genetics/*toxicity ; Bacterial Toxins/*chemistry/genetics/*toxicity ; Cell Line ; Fetal Proteins/*antagonists & inhibitors ; Intestinal Mucosa/drug effects/metabolism ; Microfilament Proteins/*antagonists & inhibitors ; Nuclear Proteins/*antagonists & inhibitors ; Polymerization/drug effects ; Protein Structure, Tertiary ; Rats
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The final countdown (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1188-90. doi: 10.1126/science.350.6265.1188.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785475" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/blood/genetics/*physiology ; Animals ; Biological Clocks/genetics/*physiology ; Biomarkers/blood/metabolism ; DNA/genetics ; DNA Methylation ; Epigenesis, Genetic ; Humans ; Mice ; Rats ; Telomere Homeostasis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    BRAIN STRUCTURE. Cortical folding scales universally with surface area and thickness, not number of neurons (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-07-04
    Description: Larger brains tend to have more folded cortices, but what makes the cortex fold has remained unknown. We show that the degree of cortical folding scales uniformly across lissencephalic and gyrencephalic species, across individuals, and within individual cortices as a function of the product of cortical surface area and the square root of cortical thickness. This relation is derived from the minimization of the effective free energy associated with cortical shape according to a simple physical model, based on known mechanisms of axonal elongation. This model also explains the scaling of the folding index of crumpled paper balls. We discuss the implications of this finding for the evolutionary and developmental origin of folding, including the newfound continuum between lissencephaly and gyrencephaly, and for pathologies such as human lissencephaly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mota, Bruno -- Herculano-Houzel, Suzana -- New York, N.Y. -- Science. 2015 Jul 3;349(6243):74-7. doi: 10.1126/science.aaa9101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto de Fisica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. ; Instituto de Ciencias Biomedicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil. Instituto Nacional de Neurociencia Translacional, INCT/MCT, Sao Paulo, Brazil. suzanahh@gmail.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26138976" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; *Cerebral Cortex/cytology/embryology/pathology ; Humans ; Lissencephaly/*pathology ; Mice ; Models, Neurological ; Neurons/*cytology/pathology ; Rats ; Species Specificity
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    Neuroscience. Our skewed sense of space (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buzsaki, Gyorgy -- New York, N.Y. -- Science. 2015 Feb 6;347(6222):612-3. doi: 10.1126/science.aaa6505.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉New York University Neuroscience Institute, New York University Langone Center, New York, NY 10016, USA. gyorgy.buzsaki@nyumc.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25657232" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Hippocampus/*physiology ; Maze Learning ; Pyramidal Cells/*physiology ; Rats ; Sensation/*physiology ; Space Perception/*physiology
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    CTCF establishes discrete functional chromatin domains at the Hox clusters during differentiation (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-02-28
    Description: Polycomb and Trithorax group proteins encode the epigenetic memory of cellular positional identity by establishing inheritable domains of repressive and active chromatin within the Hox clusters. Here we demonstrate that the CCCTC-binding factor (CTCF) functions to insulate these adjacent yet antagonistic chromatin domains during embryonic stem cell differentiation into cervical motor neurons. Deletion of CTCF binding sites within the Hox clusters results in the expansion of active chromatin into the repressive domain. CTCF functions as an insulator by organizing Hox clusters into spatially disjoint domains. Ablation of CTCF binding disrupts topological boundaries such that caudal Hox genes leave the repressed domain and become subject to transcriptional activation. Hence, CTCF is required to insulate facultative heterochromatin from impinging euchromatin to produce discrete positional identities.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428148/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428148/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Narendra, Varun -- Rocha, Pedro P -- An, Disi -- Raviram, Ramya -- Skok, Jane A -- Mazzoni, Esteban O -- Reinberg, Danny -- GM-64844/GM/NIGMS NIH HHS/ -- GM086852/GM/NIGMS NIH HHS/ -- GM112192/GM/NIGMS NIH HHS/ -- P30 CA016087/CA/NCI NIH HHS/ -- R01 GM086852/GM/NIGMS NIH HHS/ -- R01 GM112192/GM/NIGMS NIH HHS/ -- R01 HD079682/HD/NICHD NIH HHS/ -- R01HD079682/HD/NICHD NIH HHS/ -- R37-37120/PHS HHS/ -- T32 GM007238/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Feb 27;347(6225):1017-21. doi: 10.1126/science.1262088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY 10016, USA. ; Department of Pathology, New York University School of Medicine, New York, NY 10016, USA. ; Department of Biology, New York University, New York, NY 10003, USA. ; Department of Biology, New York University, New York, NY 10003, USA. danny.reinberg@nyumc.org eom204@nyu.edu. ; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY 10016, USA. danny.reinberg@nyumc.org eom204@nyu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25722416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/*genetics ; Chromatin/chemistry/genetics/*metabolism ; Dogs ; Embryonic Stem Cells/*cytology ; *Gene Expression Regulation ; *Genes, Homeobox ; Humans ; Mice ; Motor Neurons/*cytology ; Multigene Family ; Neck ; Protein Structure, Tertiary ; Rats ; Repressor Proteins/chemistry/genetics/*metabolism
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    STEM CELLS. NIH debates human-animal chimeras (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-10-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2015 Oct 16;350(6258):261-2. doi: 10.1126/science.350.6258.261.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26472885" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; *Chimera ; *Embryonic Stem Cells ; *Financing, Organized ; Humans ; Mice ; National Institutes of Health (U.S.)/*economics ; Organ Transplantation ; Rats ; Stem Cell Research/*economics ; Swine ; United States
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    SYNTHETIC BIOLOGY. Modified yeast produce opiates from sugar (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-08-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, Robert F -- New York, N.Y. -- Science. 2015 Aug 14;349(6249):677. doi: 10.1126/science.349.6249.677.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26273032" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Opioid/*metabolism ; Animals ; Carbohydrates ; *Genetic Engineering ; Papaver/genetics/*metabolism ; Rats ; Saccharomyces cerevisiae/genetics/*metabolism ; Synthetic Biology
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    Wireless magnetothermal deep brain stimulation (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-03-15
    Description: Wireless deep brain stimulation of well-defined neuronal populations could facilitate the study of intact brain circuits and the treatment of neurological disorders. Here, we demonstrate minimally invasive and remote neural excitation through the activation of the heat-sensitive capsaicin receptor TRPV1 by magnetic nanoparticles. When exposed to alternating magnetic fields, the nanoparticles dissipate heat generated by hysteresis, triggering widespread and reversible firing of TRPV1(+) neurons. Wireless magnetothermal stimulation in the ventral tegmental area of mice evoked excitation in subpopulations of neurons in the targeted brain region and in structures receiving excitatory projections. The nanoparticles persisted in the brain for over a month, allowing for chronic stimulation without the need for implants and connectors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Ritchie -- Romero, Gabriela -- Christiansen, Michael G -- Mohr, Alan -- Anikeeva, Polina -- New York, N.Y. -- Science. 2015 Mar 27;347(6229):1477-80. doi: 10.1126/science.1261821. Epub 2015 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Research Laboratory of Electronics, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Research Laboratory of Electronics, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Department of Chemical Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Department of Materials Science and Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Research Laboratory of Electronics, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. anikeeva@mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25765068" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Deep Brain Stimulation/*methods ; Evoked Potentials ; HEK293 Cells ; Humans ; *Magnetite Nanoparticles ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/physiology ; Rats ; TRPV Cation Channels/agonists ; Ventral Tegmental Area/physiology ; *Wireless Technology
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    Bioelectronics. A soft approach kick-starts cybernetic implants (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-01-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Service, Robert F -- New York, N.Y. -- Science. 2015 Jan 9;347(6218):114. doi: 10.1126/science.347.6218.114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25573999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bionics ; *Electrodes, Implanted ; Movement ; Paralysis/physiopathology/*therapy ; Rats ; Sensation ; Spinal Cord Injuries/physiopathology/*therapy ; *Walking
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    Brain computation. Selective information routing by ventral hippocampal CA1 projection neurons (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-02
    Description: The hippocampus computes diverse information involving spatial memory, anxiety, or reward and directly projects to several brain areas. Are different computations transmitted to all downstream targets uniformly, or does the hippocampus selectively route information according to content and target region? By recording from ventral hippocampal CA1 neurons in rats during different behavioral tasks and determining axonal projections with optogenetics, we observed subsets of neurons changing firing at places of elevated anxiety or changing activity during goal approach. Anxiety-related firing was selectively increased in neurons projecting to the prefrontal cortex. Goal-directed firing was most prominent in neurons targeting the nucleus accumbens; and triple-projecting neurons, targeting the prefrontal cortex, amygdala, and nucleus accumbens, were most active during tasks and sharp wave/ripples. Thus, hippocampal neurons route distinct behavior-contingent information selectively to different target areas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ciocchi, S -- Passecker, J -- Malagon-Vina, H -- Mikus, N -- Klausberger, T -- New York, N.Y. -- Science. 2015 May 1;348(6234):560-3. doi: 10.1126/science.aaa3245.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Brain Research, Department for Cognitive Neurobiology, Medical University Vienna, Spitalgasse 4, 1090 Vienna, Austria. stephane.ciocchi@meduniwien.ac.at thomas.klausberger@meduniwien.ac.at. ; Center for Brain Research, Department for Cognitive Neurobiology, Medical University Vienna, Spitalgasse 4, 1090 Vienna, Austria. ; Center for Brain Research, Department for Cognitive Neurobiology, Medical University Vienna, Spitalgasse 4, 1090 Vienna, Austria. Medical Research Council, Anatomical Neuropharmacology Unit, Oxford University, Mansfield Road, Oxford OX1 3TH, UK. stephane.ciocchi@meduniwien.ac.at thomas.klausberger@meduniwien.ac.at.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25931556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/physiopathology ; CA1 Region, Hippocampal/*physiology ; Cell Communication ; Male ; Mental Processes/*physiology ; Neurons/physiology ; Nucleus Accumbens/physiology ; Optogenetics ; Prefrontal Cortex/physiology ; Rats ; Rats, Inbred LEC ; *Spatial Learning
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    Structural biology. Structural basis for Notch1 engagement of Delta-like 4 (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-02-24
    Description: Notch receptors guide mammalian cell fate decisions by engaging the proteins Jagged and Delta-like (DLL). The 2.3 angstrom resolution crystal structure of the interacting regions of the Notch1-DLL4 complex reveals a two-site, antiparallel binding orientation assisted by Notch1 O-linked glycosylation. Notch1 epidermal growth factor-like repeats 11 and 12 interact with the DLL4 Delta/Serrate/Lag-2 (DSL) domain and module at the N-terminus of Notch ligands (MNNL) domains, respectively. Threonine and serine residues on Notch1 are functionalized with O-fucose and O-glucose, which act as surrogate amino acids by making specific, and essential, contacts to residues on DLL4. The elucidation of a direct chemical role for O-glycans in Notch1 ligand engagement demonstrates how, by relying on posttranslational modifications of their ligand binding sites, Notch proteins have linked their functional capacity to developmentally regulated biosynthetic pathways.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445638/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4445638/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luca, Vincent C -- Jude, Kevin M -- Pierce, Nathan W -- Nachury, Maxence V -- Fischer, Suzanne -- Garcia, K Christopher -- 1R01-GM097015/GM/NIGMS NIH HHS/ -- R01 GM097015/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Feb 20;347(6224):847-53. doi: 10.1126/science.1261093.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. ; Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305, USA. kcgarcia@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25700513" target="_blank"〉PubMed〈/a〉
    Keywords: Alagille Syndrome/genetics ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Cell Line ; Conserved Sequence ; Crystallography, X-Ray ; Fucose/chemistry ; Glucose/chemistry ; Glycosylation ; Intracellular Signaling Peptides and Proteins/*chemistry/genetics ; Ligands ; Membrane Proteins/*chemistry/genetics/ultrastructure ; Molecular Sequence Data ; Molecular Targeted Therapy ; Polysaccharides/chemistry ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/genetics ; Protein Binding ; Protein Structure, Tertiary ; Rats ; Receptor, Notch1/*chemistry/genetics/ultrastructure ; Serine/chemistry/genetics ; Threonine/chemistry/genetics
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    Spatial navigation. Disruption of the head direction cell network impairs the parahippocampal grid cell signal (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-02-24
    Description: Navigation depends on multiple neural systems that encode the moment-to-moment changes in an animal's direction and location in space. These include head direction (HD) cells representing the orientation of the head and grid cells that fire at multiple locations, forming a repeating hexagonal grid pattern. Computational models hypothesize that generation of the grid cell signal relies upon HD information that ascends to the hippocampal network via the anterior thalamic nuclei (ATN). We inactivated or lesioned the ATN and subsequently recorded single units in the entorhinal cortex and parasubiculum. ATN manipulation significantly disrupted grid and HD cell characteristics while sparing theta rhythmicity in these regions. These results indicate that the HD signal via the ATN is necessary for the generation and function of grid cell activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4476794/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4476794/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Winter, Shawn S -- Clark, Benjamin J -- Taube, Jeffrey S -- NS053907/NS/NINDS NIH HHS/ -- R01 MH048924/MH/NIMH NIH HHS/ -- R01 NS053907/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2015 Feb 20;347(6224):870-4. doi: 10.1126/science.1259591. Epub 2015 Feb 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychological and Brain Sciences, Center for Cognitive Neuroscience, Dartmouth College, Hanover, NH 03755, USA. ; Department of Psychological and Brain Sciences, Center for Cognitive Neuroscience, Dartmouth College, Hanover, NH 03755, USA. jeffrey.taube@dartmouth.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25700518" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Thalamic Nuclei/drug effects/*physiology ; Entorhinal Cortex/cytology/*physiology ; Female ; Head ; Hippocampus/cytology/physiology ; Lidocaine/pharmacology ; Nerve Net/cytology/drug effects/*physiology ; Neurons/*physiology ; Orientation/*physiology ; Rats ; Rats, Inbred LEC ; Signal Transduction ; Spatial Navigation/*physiology ; Theta Rhythm
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    Regenerative medicine. 'Rejuvenating' protein doubted (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaiser, Jocelyn -- New York, N.Y. -- Science. 2015 May 22;348(6237):849. doi: 10.1126/science.348.6237.849.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25999487" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/blood ; Animals ; Biological Assay ; *Blood ; Bone Morphogenetic Proteins/blood/pharmacology/*physiology ; Brain/drug effects/physiology ; Growth Differentiation Factors/blood/pharmacology/*physiology ; Heart/drug effects/physiology ; Mice ; Muscle, Skeletal/drug effects/physiology ; Myostatin/pharmacology/physiology ; Parabiosis ; Rats ; Regeneration/drug effects ; *Rejuvenation
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    Transcribed enhancers lead waves of coordinated transcription in transitioning mammalian cells (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-02-14
    Description: Although it is generally accepted that cellular differentiation requires changes to transcriptional networks, dynamic regulation of promoters and enhancers at specific sets of genes has not been previously studied en masse. Exploiting the fact that active promoters and enhancers are transcribed, we simultaneously measured their activity in 19 human and 14 mouse time courses covering a wide range of cell types and biological stimuli. Enhancer RNAs, then messenger RNAs encoding transcription factors, dominated the earliest responses. Binding sites for key lineage transcription factors were simultaneously overrepresented in enhancers and promoters active in each cellular system. Our data support a highly generalizable model in which enhancer transcription is the earliest event in successive waves of transcriptional change during cellular differentiation or activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4681433/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4681433/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arner, Erik -- Daub, Carsten O -- Vitting-Seerup, Kristoffer -- Andersson, Robin -- Lilje, Berit -- Drablos, Finn -- Lennartsson, Andreas -- Ronnerblad, Michelle -- Hrydziuszko, Olga -- Vitezic, Morana -- Freeman, Tom C -- Alhendi, Ahmad M N -- Arner, Peter -- Axton, Richard -- Baillie, J Kenneth -- Beckhouse, Anthony -- Bodega, Beatrice -- Briggs, James -- Brombacher, Frank -- Davis, Margaret -- Detmar, Michael -- Ehrlund, Anna -- Endoh, Mitsuhiro -- Eslami, Afsaneh -- Fagiolini, Michela -- Fairbairn, Lynsey -- Faulkner, Geoffrey J -- Ferrai, Carmelo -- Fisher, Malcolm E -- Forrester, Lesley -- Goldowitz, Daniel -- Guler, Reto -- Ha, Thomas -- Hara, Mitsuko -- Herlyn, Meenhard -- Ikawa, Tomokatsu -- Kai, Chieko -- Kawamoto, Hiroshi -- Khachigian, Levon M -- Klinken, S Peter -- Kojima, Soichi -- Koseki, Haruhiko -- Klein, Sarah -- Mejhert, Niklas -- Miyaguchi, Ken -- Mizuno, Yosuke -- Morimoto, Mitsuru -- Morris, Kelly J -- Mummery, Christine -- Nakachi, Yutaka -- Ogishima, Soichi -- Okada-Hatakeyama, Mariko -- Okazaki, Yasushi -- Orlando, Valerio -- Ovchinnikov, Dmitry -- Passier, Robert -- Patrikakis, Margaret -- Pombo, Ana -- Qin, Xian-Yang -- Roy, Sugata -- Sato, Hiroki -- Savvi, Suzana -- Saxena, Alka -- Schwegmann, Anita -- Sugiyama, Daisuke -- Swoboda, Rolf -- Tanaka, Hiroshi -- Tomoiu, Andru -- Winteringham, Louise N -- Wolvetang, Ernst -- Yanagi-Mizuochi, Chiyo -- Yoneda, Misako -- Zabierowski, Susan -- Zhang, Peter -- Abugessaisa, Imad -- Bertin, Nicolas -- Diehl, Alexander D -- Fukuda, Shiro -- Furuno, Masaaki -- Harshbarger, Jayson -- Hasegawa, Akira -- Hori, Fumi -- Ishikawa-Kato, Sachi -- Ishizu, Yuri -- Itoh, Masayoshi -- Kawashima, Tsugumi -- Kojima, Miki -- Kondo, Naoto -- Lizio, Marina -- Meehan, Terrence F -- Mungall, Christopher J -- Murata, Mitsuyoshi -- Nishiyori-Sueki, Hiromi -- Sahin, Serkan -- Nagao-Sato, Sayaka -- Severin, Jessica -- de Hoon, Michiel J L -- Kawai, Jun -- Kasukawa, Takeya -- Lassmann, Timo -- Suzuki, Harukazu -- Kawaji, Hideya -- Summers, Kim M -- Wells, Christine -- FANTOM Consortium -- Hume, David A -- Forrest, Alistair R R -- Sandelin, Albin -- Carninci, Piero -- Hayashizaki, Yoshihide -- P30 CA010815/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2015 Feb 27;347(6225):1010-4. doi: 10.1126/science.1259418. Epub 2015 Feb 12.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25678556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cattle ; Cell Differentiation/*genetics ; Dogs ; *Enhancer Elements, Genetic ; *Gene Expression Regulation, Developmental ; Mice ; RNA, Messenger/genetics/metabolism ; Rats ; Stem Cells/*cytology/metabolism ; Transcription Factors/*metabolism ; *Transcription, Genetic
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    Proteasomes. A molecular census of 26S proteasomes in intact neurons (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-01-24
    Description: The 26S proteasome is a key player in eukaryotic protein quality control and in the regulation of numerous cellular processes. Here, we describe quantitative in situ structural studies of this highly dynamic molecular machine in intact hippocampal neurons. We used electron cryotomography with the Volta phase plate, which allowed high fidelity and nanometer precision localization of 26S proteasomes. We undertook a molecular census of single- and double-capped proteasomes and assessed the conformational states of individual complexes. Under the conditions of the experiment-that is, in the absence of proteotoxic stress-only 20% of the 26S proteasomes were engaged in substrate processing. The remainder was in the substrate-accepting ground state. These findings suggest that in the absence of stress, the capacity of the proteasome system is not fully used.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Asano, Shoh -- Fukuda, Yoshiyuki -- Beck, Florian -- Aufderheide, Antje -- Forster, Friedrich -- Danev, Radostin -- Baumeister, Wolfgang -- New York, N.Y. -- Science. 2015 Jan 23;347(6220):439-42. doi: 10.1126/science.1261197.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Structural Biology, Max-Planck Institute of Biochemistry, 82152 Martinsried, Germany. ; Department of Molecular Structural Biology, Max-Planck Institute of Biochemistry, 82152 Martinsried, Germany. baumeist@biochem.mpg.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25613890" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Hippocampus/*cytology/enzymology ; Neurons/*enzymology/*ultrastructure ; Proteasome Endopeptidase Complex/*chemistry ; Protein Conformation ; Rats ; Stress, Physiological
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    Controlled-release mitochondrial protonophore reverses diabetes and steatohepatitis in rats (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-02-28
    Description: Nonalcoholic fatty liver disease (NAFLD) is a major factor in the pathogenesis of type 2 diabetes (T2D) and nonalcoholic steatohepatitis (NASH). The mitochondrial protonophore 2,4 dinitrophenol (DNP) has beneficial effects on NAFLD, insulin resistance, and obesity in preclinical models but is too toxic for clinical use. We developed a controlled-release oral formulation of DNP, called CRMP (controlled-release mitochondrial protonophore), that produces mild hepatic mitochondrial uncoupling. In rat models, CRMP reduced hypertriglyceridemia, insulin resistance, hepatic steatosis, and diabetes. It also normalized plasma transaminase concentrations, ameliorated liver fibrosis, and improved hepatic protein synthetic function in a methionine/choline-deficient rat model of NASH. Chronic treatment with CRMP was not associated with any systemic toxicity. These data offer proof of concept that mild hepatic mitochondrial uncoupling may be a safe and effective therapy for the related epidemics of metabolic syndrome, T2D, and NASH.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4495920/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4495920/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perry, Rachel J -- Zhang, Dongyan -- Zhang, Xian-Man -- Boyer, James L -- Shulman, Gerald I -- P30 DK-34989/DK/NIDDK NIH HHS/ -- P30 DK-45735/DK/NIDDK NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- P30 DK045735/DK/NIDDK NIH HHS/ -- R01 DK-40936/DK/NIDDK NIH HHS/ -- R01 DK040936/DK/NIDDK NIH HHS/ -- R24 DK-085638/DK/NIDDK NIH HHS/ -- T32 DK-101019/DK/NIDDK NIH HHS/ -- U24 DK-059635/DK/NIDDK NIH HHS/ -- UL1 TR-000142/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Mar 13;347(6227):1253-6. doi: 10.1126/science.aaa0672. Epub 2015 Feb 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA. Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA. ; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA. ; Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. ; Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. Yale Liver Center, Yale University School of Medicine, New Haven, CT, USA. ; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT, USA. Departments of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA. Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA. gerald.shulman@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25721504" target="_blank"〉PubMed〈/a〉
    Keywords: 2,4-Dinitrophenol/*administration & dosage/toxicity ; Animals ; Blood Glucose/metabolism ; Delayed-Action Preparations/*administration & dosage ; Diabetes Mellitus, Type 2/*drug therapy/metabolism ; Glucose Tolerance Test ; Insulin Resistance ; Lipid Metabolism ; Liver Cirrhosis/drug therapy ; Male ; Mice ; Mitochondria, Liver/drug effects/metabolism ; Muscle, Skeletal/metabolism ; Non-alcoholic Fatty Liver Disease/*drug therapy/metabolism ; Oxidation-Reduction ; Proton Ionophores/*administration & dosage/toxicity ; Random Allocation ; Rats ; Rats, Zucker
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    PLACE CELLS. Autoassociative dynamics in the generation of sequences of hippocampal place cells (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-07-15
    Description: Neuronal circuits produce self-sustaining sequences of activity patterns, but the precise mechanisms remain unknown. Here we provide evidence for autoassociative dynamics in sequence generation. During sharp-wave ripple (SWR) events, hippocampal neurons express sequenced reactivations, which we show are composed of discrete attractors. Each attractor corresponds to a single location, the representation of which sharpens over the course of several milliseconds, as the reactivation focuses at that location. Subsequently, the reactivation transitions rapidly to a spatially discontiguous location. This alternation between sharpening and transition occurs repeatedly within individual SWRs and is locked to the slow-gamma (25 to 50 hertz) rhythm. These findings support theoretical notions of neural network function and reveal a fundamental discretization in the retrieval of memory in the hippocampus, together with a function for gamma oscillations in the control of attractor dynamics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfeiffer, Brad E -- Foster, David J -- New York, N.Y. -- Science. 2015 Jul 10;349(6244):180-3. doi: 10.1126/science.aaa9633.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA. ; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA. david.foster@jhu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26160946" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gamma Rhythm ; Hippocampus/*cytology/*physiology ; Male ; Mental Recall/*physiology ; Neural Pathways ; Neurons/*physiology ; Rats ; Rats, Inbred LEC
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    Toxicology. A child-killing toxin emerges from shadows (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-04-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pulla, Priyanka -- New York, N.Y. -- Science. 2015 Apr 3;348(6230):15-6. doi: 10.1126/science.348.6230.15.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25838358" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Animals ; Blood Glucose ; *Cause of Death ; Child ; *Child Mortality ; Child, Preschool ; Coma/etiology/mortality ; Cyclopropanes/*toxicity ; Death, Sudden/etiology ; Eating ; Encephalitis/etiology/mortality ; Glucose/administration & dosage ; Glycine/*analogs & derivatives/toxicity ; Humans ; Hypoglycemia/drug therapy/*etiology/*mortality ; India/epidemiology ; Litchi/*toxicity ; Memory Disorders/etiology ; Mental Disorders/etiology ; Rats ; Seizures/etiology ; Toxins, Biological/*toxicity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    REGENERATIVE MEDICINE. California stem cell agency plots a race to the clinic (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Servick, Kelly -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):15. doi: 10.1126/science.351.6268.15.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721984" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; California ; Cell Differentiation ; Clinical Trials as Topic ; Drug Industry ; Embryonic Stem Cells/cytology/*transplantation ; Financing, Organized ; Humans ; Photoreceptor Cells/physiology ; Rats ; Regenerative Medicine/*economics/*trends ; Retina/cytology/physiology ; Stem Cell Research/*economics
    Print ISSN: 0036-8075
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    Sequential ionic and conformational signaling by calcium channels drives neuronal gene expression (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-02-26
    Description: Voltage-gated CaV1.2 channels (L-type calcium channel alpha1C subunits) are critical mediators of transcription-dependent neural plasticity. Whether these channels signal via the influx of calcium ion (Ca(2+)), voltage-dependent conformational change (VDeltaC), or a combination of the two has thus far been equivocal. We fused CaV1.2 to a ligand-gated Ca(2+)-permeable channel, enabling independent control of localized Ca(2+) and VDeltaC signals. This revealed an unexpected dual requirement: Ca(2+) must first mobilize actin-bound Ca(2+)/calmodulin-dependent protein kinase II, freeing it for subsequent VDeltaC-mediated accumulation. Neither signal alone sufficed to activate transcription. Signal order was crucial: Efficiency peaked when Ca(2+) preceded VDeltaC by 10 to 20 seconds. CaV1.2 VDeltaC synergistically augmented signaling by N-methyl-d-aspartate receptors. Furthermore, VDeltaC mistuning correlated with autistic symptoms in Timothy syndrome. Thus, nonionic VDeltaC signaling is vital to the function of CaV1.2 in synaptic and neuropsychiatric processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Boxing -- Tadross, Michael R -- Tsien, Richard W -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):863-7. doi: 10.1126/science.aad3647.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. ; Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA. Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA. tadrossm@janelia.hhmi.org. ; Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/chemistry/*metabolism ; *Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; *Gene Expression Regulation ; HEK293 Cells ; Hippocampus/cytology ; Humans ; Long QT Syndrome/genetics/metabolism ; Neuronal Plasticity/*genetics ; Neurons/drug effects/*metabolism ; Nimodipine/pharmacology ; Protein Conformation/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism ; Syndactyly/genetics/metabolism
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    Prefrontal cortical regulation of brainwide circuit dynamics and reward-related behavior (2016)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2016-01-02
    Description: Motivation for reward drives adaptive behaviors, whereas impairment of reward perception and experience (anhedonia) can contribute to psychiatric diseases, including depression and schizophrenia. We sought to test the hypothesis that the medial prefrontal cortex (mPFC) controls interactions among specific subcortical regions that govern hedonic responses. By using optogenetic functional magnetic resonance imaging to locally manipulate but globally visualize neural activity in rats, we found that dopamine neuron stimulation drives striatal activity, whereas locally increased mPFC excitability reduces this striatal response and inhibits the behavioral drive for dopaminergic stimulation. This chronic mPFC overactivity also stably suppresses natural reward-motivated behaviors and induces specific new brainwide functional interactions, which predict the degree of anhedonia in individuals. These findings describe a mechanism by which mPFC modulates expression of reward-seeking behavior, by regulating the dynamical interactions between specific distant subcortical regions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772156/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772156/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferenczi, Emily A -- Zalocusky, Kelly A -- Liston, Conor -- Grosenick, Logan -- Warden, Melissa R -- Amatya, Debha -- Katovich, Kiefer -- Mehta, Hershel -- Patenaude, Brian -- Ramakrishnan, Charu -- Kalanithi, Paul -- Etkin, Amit -- Knutson, Brian -- Glover, Gary H -- Deisseroth, Karl -- 1F31MH105151_01/MH/NIMH NIH HHS/ -- P41 EB015891/EB/NIBIB NIH HHS/ -- R00 MH097822/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):aac9698. doi: 10.1126/science.aac9698.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. Neurosciences Program, Stanford University, Stanford, CA 94305, USA. ; Brain Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA. ; Department of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853, USA. ; Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. ; Department of Psychology, Stanford University, Stanford, CA 94305, USA. ; Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA 94305, USA. ; Department of Neurosurgery, Stanford University, Stanford, CA 94305, USA. ; Department of Radiology, Stanford University, Stanford, CA, 94305, USA. ; Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. Department of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853, USA. Howard Hughes Medical Institute, Stanford University, Stanford, CA, 94305, USA. deissero@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26722001" target="_blank"〉PubMed〈/a〉
    Keywords: Anhedonia/*physiology ; Animals ; Brain Mapping ; Corpus Striatum/cytology/drug effects/*physiology ; Depressive Disorder/physiopathology ; Dopamine/pharmacology ; Dopaminergic Neurons/drug effects/*physiology ; Female ; Magnetic Resonance Imaging ; Male ; Mesencephalon/cytology/drug effects/physiology ; *Motivation ; Nerve Net/physiology ; Oxygen/blood ; Prefrontal Cortex/cytology/drug effects/*physiology ; Rats ; Rats, Inbred LEC ; Rats, Sprague-Dawley ; *Reward ; Schizophrenia/physiopathology
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    Unconventional endocannabinoid signaling governs sperm activation via the sex hormone progesterone (2016)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2016-03-19
    Description: Steroids regulate cell proliferation, tissue development, and cell signaling via two pathways: a nuclear receptor mechanism and genome-independent signaling. Sperm activation, egg maturation, and steroid-induced anesthesia are executed via the latter pathway, the key components of which remain unknown. Here, we present characterization of the human sperm progesterone receptor that is conveyed by the orphan enzyme alpha/beta hydrolase domain-containing protein 2 (ABHD2). We show that ABHD2 is highly expressed in spermatozoa, binds progesterone, and acts as a progesterone-dependent lipid hydrolase by depleting the endocannabinoid 2-arachidonoylglycerol (2AG) from plasma membrane. The 2AG inhibits the sperm calcium channel (CatSper), and its removal leads to calcium influx via CatSper and ensures sperm activation. This study reveals that progesterone-activated endocannabinoid depletion by ABHD2 is a general mechanism by which progesterone exerts its genome-independent action and primes sperm for fertilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Melissa R -- Mannowetz, Nadja -- Iavarone, Anthony T -- Safavi, Rojin -- Gracheva, Elena O -- Smith, James F -- Hill, Rose Z -- Bautista, Diana M -- Kirichok, Yuriy -- Lishko, Polina V -- 1S10OD020062-01/OD/NIH HHS/ -- R01 AR059385/AR/NIAMS NIH HHS/ -- R01AR059385/AR/NIAMS NIH HHS/ -- R01GM111802/GM/NIGMS NIH HHS/ -- R01HD068914/HD/NICHD NIH HHS/ -- R21HD081403/HD/NICHD NIH HHS/ -- S10RR025622/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):555-9. doi: 10.1126/science.aad6887. Epub 2016 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA. ; QB3/Chemistry Mass Spectrometry Facility, University of California, Berkeley, CA 94720, USA. ; Department of Cellular and Molecular Physiology; Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair (CNNR), Yale School of Medicine, Yale University, New Haven, CT 06536, USA. ; Department of Urology, University of California, San Francisco, CA 94143, USA. ; Department of Physiology, University of California, San Francisco, CA 94158, USA. ; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA. lishko@berkeley.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989199" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Arachidonic Acids/*deficiency ; Calcium/metabolism ; Calcium Channels/metabolism ; Calcium Signaling ; Cell Membrane/metabolism ; Endocannabinoids/*deficiency ; Fertilization ; Glycerides/*deficiency ; Humans ; Hydrolases/genetics/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Progesterone/*metabolism/pharmacology ; Rats ; Rats, Wistar ; Receptors, Progesterone/genetics/*metabolism ; Sperm Motility/drug effects/*physiology ; Spermatozoa/drug effects/metabolism/*physiology ; Young Adult
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    Diversity in neural firing dynamics supports both rigid and learned hippocampal sequences (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-03-26
    Description: Cell assembly sequences during learning are "replayed" during hippocampal ripples and contribute to the consolidation of episodic memories. However, neuronal sequences may also reflect preexisting dynamics. We report that sequences of place-cell firing in a novel environment are formed from a combination of the contributions of a rigid, predominantly fast-firing subset of pyramidal neurons with low spatial specificity and limited change across sleep-experience-sleep and a slow-firing plastic subset. Slow-firing cells, rather than fast-firing cells, gained high place specificity during exploration, elevated their association with ripples, and showed increased bursting and temporal coactivation during postexperience sleep. Thus, slow- and fast-firing neurons, although forming a continuous distribution, have different coding and plastic properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grosmark, Andres D -- Buzsaki, Gyorgy -- MH102840/MH/NIMH NIH HHS/ -- MH54671/MH/NIMH NIH HHS/ -- NS075015/NS/NINDS NIH HHS/ -- R01 MH107396/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1440-3. doi: 10.1126/science.aad1935.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Columbia University Medical Center, New York, NY 10019, USA. The Neuroscience Institute, School of Medicine, New York University, New York, NY 10016, USA. ; The Neuroscience Institute, School of Medicine, New York University, New York, NY 10016, USA. Center for Neural Science, New York University, New York, NY 10016, USA. gyorgy.buzsaki@nyumc.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013730" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Hippocampus/cytology/*physiopathology ; Learning/*physiology ; Male ; Maze Learning ; Neuronal Plasticity ; Pyramidal Cells/*physiology ; Rats ; Rats, Inbred LEC ; Sleep/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    C9orf72 is required for proper macrophage and microglial function in mice (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-03-19
    Description: Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9orf72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Decreased expression of C9orf72 is seen in expansion carriers, suggesting that loss of function may play a role in disease. We found that two independent mouse lines lacking the C9orf72 ortholog (3110043O21Rik) in all tissues developed normally and aged without motor neuron disease. Instead, C9orf72 null mice developed progressive splenomegaly and lymphadenopathy with accumulation of engorged macrophage-like cells. C9orf72 expression was highest in myeloid cells, and the loss of C9orf72 led to lysosomal accumulation and altered immune responses in macrophages and microglia, with age-related neuroinflammation similar to C9orf72 ALS but not sporadic ALS human patient tissue. Thus, C9orf72 is required for the normal function of myeloid cells, and altered microglial function may contribute to neurodegeneration in C9orf72 expansion carriers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Rourke, J G -- Bogdanik, L -- Yanez, A -- Lall, D -- Wolf, A J -- Muhammad, A K M G -- Ho, R -- Carmona, S -- Vit, J P -- Zarrow, J -- Kim, K J -- Bell, S -- Harms, M B -- Miller, T M -- Dangler, C A -- Underhill, D M -- Goodridge, H S -- Lutz, C M -- Baloh, R H -- GM085796/GM/NIGMS NIH HHS/ -- NS069669/NS/NINDS NIH HHS/ -- NS078398/NS/NINDS NIH HHS/ -- NS087351/NS/NINDS NIH HHS/ -- UL1TR000124/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1324-9. doi: 10.1126/science.aaf1064.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. ; The Jackson Laboratory, Bar Harbor, ME, USA. ; Division of Biomedical Sciences, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. ; Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. ; Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. Department of Neurology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989253" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/immunology ; Amyotrophic Lateral Sclerosis/genetics/*immunology ; Animals ; Frontotemporal Dementia/genetics/*immunology ; Gene Knockdown Techniques ; Guanine Nucleotide Exchange Factors/genetics/*physiology ; Heterozygote ; Humans ; Lymphatic Diseases/genetics/immunology ; Macrophages/*immunology ; Mice ; Mice, Knockout ; Microglia/*immunology ; Myeloid Cells/*immunology ; Proteins/genetics/*physiology ; Rats ; Splenomegaly/genetics/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    CLK2 inhibition ameliorates autistic features associated with SHANK3 deficiency (2016)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2016-02-06
    Description: SH3 and multiple ankyrin repeat domains 3 (SHANK3) haploinsufficiency is causative for the neurological features of Phelan-McDermid syndrome (PMDS), including a high risk of autism spectrum disorder (ASD). We used unbiased, quantitative proteomics to identify changes in the phosphoproteome of Shank3-deficient neurons. Down-regulation of protein kinase B (PKB/Akt)-mammalian target of rapamycin complex 1 (mTORC1) signaling resulted from enhanced phosphorylation and activation of serine/threonine protein phosphatase 2A (PP2A) regulatory subunit, B56beta, due to increased steady-state levels of its kinase, Cdc2-like kinase 2 (CLK2). Pharmacological and genetic activation of Akt or inhibition of CLK2 relieved synaptic deficits in Shank3-deficient and PMDS patient-derived neurons. CLK2 inhibition also restored normal sociability in a Shank3-deficient mouse model. Our study thereby provides a novel mechanistic and potentially therapeutic understanding of deregulated signaling downstream of Shank3 deficiency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bidinosti, Michael -- Botta, Paolo -- Kruttner, Sebastian -- Proenca, Catia C -- Stoehr, Natacha -- Bernhard, Mario -- Fruh, Isabelle -- Mueller, Matthias -- Bonenfant, Debora -- Voshol, Hans -- Carbone, Walter -- Neal, Sarah J -- McTighe, Stephanie M -- Roma, Guglielmo -- Dolmetsch, Ricardo E -- Porter, Jeffrey A -- Caroni, Pico -- Bouwmeester, Tewis -- Luthi, Andreas -- Galimberti, Ivan -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1199-203. doi: 10.1126/science.aad5487. Epub 2016 Feb 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Molecular Pathways, Novartis Institutes for Biomedical Research, Basel, Switzerland. ; Friedrich Miescher Institute, Basel, Switzerland. ; Analytical Sciences and Imaging, Novartis Institutes for Biomedical Research, Basel, Switzerland. ; Neuroscience, Novartis Institutes for Biomedical Research, Cambridge, USA. ; Developmental Molecular Pathways, Novartis Institutes for Biomedical Research, Basel, Switzerland. ivan.galimberti@novartis.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26847545" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Autism Spectrum Disorder/*drug therapy/enzymology/genetics ; Chromosome Deletion ; Chromosome Disorders/genetics ; Chromosomes, Human, Pair 22/genetics ; Disease Models, Animal ; Down-Regulation ; Gene Knockdown Techniques ; Humans ; Insulin-Like Growth Factor I/metabolism ; Mice ; Molecular Sequence Data ; Multiprotein Complexes/metabolism ; Nerve Tissue Proteins/*genetics ; Neurons/enzymology ; Phosphorylation ; Protein Phosphatase 2/metabolism ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/metabolism ; Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Proteomics ; Proto-Oncogene Proteins c-akt/genetics/metabolism ; Rats ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Detyrosinated microtubules buckle and bear load in contracting cardiomyocytes (2016)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2016-04-23
    Description: The microtubule (MT) cytoskeleton can transmit mechanical signals and resist compression in contracting cardiomyocytes. How MTs perform these roles remains unclear because of difficulties in observing MTs during the rapid contractile cycle. Here, we used high spatial and temporal resolution imaging to characterize MT behavior in beating mouse myocytes. MTs deformed under contractile load into sinusoidal buckles, a behavior dependent on posttranslational "detyrosination" of alpha-tubulin. Detyrosinated MTs associated with desmin at force-generating sarcomeres. When detyrosination was reduced, MTs uncoupled from sarcomeres and buckled less during contraction, which allowed sarcomeres to shorten and stretch with less resistance. Conversely, increased detyrosination promoted MT buckling, stiffened the myocyte, and correlated with impaired function in cardiomyopathy. Thus, detyrosinated MTs represent tunable, compression-resistant elements that may impair cardiac function in disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robison, Patrick -- Caporizzo, Matthew A -- Ahmadzadeh, Hossein -- Bogush, Alexey I -- Chen, Christina Yingxian -- Margulies, Kenneth B -- Shenoy, Vivek B -- Prosser, Benjamin L -- HL089847/HL/NHLBI NIH HHS/ -- HL105993/HL/NHLBI NIH HHS/ -- R00-HL114879/HL/NHLBI NIH HHS/ -- R01EB017753/EB/NIBIB NIH HHS/ -- T32AR053461-09/AR/NIAMS NIH HHS/ -- T32HL007954/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):aaf0659. doi: 10.1126/science.aaf0659.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Pennsylvania Muscle Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. ; Department of Materials Science and Engineering, University of Pennsylvania School of Engineering and Applied Science, Philadelphia, PA 19104, USA. ; Department of Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. ; Department of Physiology, Pennsylvania Muscle Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. bpros@mail.med.upenn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Desmin/metabolism ; Elasticity ; Heart Failure/metabolism/physiopathology ; Humans ; Male ; Mice ; Microtubules/*metabolism ; Models, Biological ; *Myocardial Contraction ; Myocytes, Cardiac/metabolism/*physiology ; Peptide Synthases/genetics/metabolism ; *Protein Processing, Post-Translational ; RNA, Small Interfering/genetics ; Rats ; Rats, Sprague-Dawley ; Sarcomeres/metabolism ; Tubulin/*metabolism ; Tyrosine/*metabolism
    Print ISSN: 0036-8075
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    Bioresorbable silicon electronic sensors for the brain (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-01-19
    Description: Many procedures in modern clinical medicine rely on the use of electronic implants in treating conditions that range from acute coronary events to traumatic injury. However, standard permanent electronic hardware acts as a nidus for infection: bacteria form biofilms along percutaneous wires, or seed haematogenously, with the potential to migrate within the body and to provoke immune-mediated pathological tissue reactions. The associated surgical retrieval procedures, meanwhile, subject patients to the distress associated with re-operation and expose them to additional complications. Here, we report materials, device architectures, integration strategies, and in vivo demonstrations in rats of implantable, multifunctional silicon sensors for the brain, for which all of the constituent materials naturally resorb via hydrolysis and/or metabolic action, eliminating the need for extraction. Continuous monitoring of intracranial pressure and temperature illustrates functionality essential to the treatment of traumatic brain injury; the measurement performance of our resorbable devices compares favourably with that of non-resorbable clinical standards. In our experiments, insulated percutaneous wires connect to an externally mounted, miniaturized wireless potentiostat for data transmission. In a separate set-up, we connect a sensor to an implanted (but only partially resorbable) data-communication system, proving the principle that there is no need for any percutaneous wiring. The devices can be adapted to sense fluid flow, motion, pH or thermal characteristics, in formats that are compatible with the body's abdomen and extremities, as well as the deep brain, suggesting that the sensors might meet many needs in clinical medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Seung-Kyun -- Murphy, Rory K J -- Hwang, Suk-Won -- Lee, Seung Min -- Harburg, Daniel V -- Krueger, Neil A -- Shin, Jiho -- Gamble, Paul -- Cheng, Huanyu -- Yu, Sooyoun -- Liu, Zhuangjian -- McCall, Jordan G -- Stephen, Manu -- Ying, Hanze -- Kim, Jeonghyun -- Park, Gayoung -- Webb, R Chad -- Lee, Chi Hwan -- Chung, Sangjin -- Wie, Dae Seung -- Gujar, Amit D -- Vemulapalli, Bharat -- Kim, Albert H -- Lee, Kyung-Mi -- Cheng, Jianjun -- Huang, Younggang -- Lee, Sang Hoon -- Braun, Paul V -- Ray, Wilson Z -- Rogers, John A -- F31MH101956/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Feb 4;530(7588):71-6. doi: 10.1038/nature16492. Epub 2016 Jan 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA. ; Frederick Seitz Materials Research Laboratory, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA. ; Department of Neurological Surgery, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; KU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul 136-701, Republic of Korea. ; Department of Chemical and Biomolecular Engineering, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA. ; Department of Engineering Science and Mechanics, Materials Research Institute, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. ; Institute of High Performance Computing, Singapore 138632, Singapore. ; Department of Anesthesiology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Department of Biomicrosystem Technology, Korea University, Seoul 136-701, South Korea. ; Department of Biochemistry and Molecular Biology, Korea University College of Medicine, Seoul 136-713, South Korea. ; Weldon School of Biomedical Engineering, School of Mechanical Engineering, The Center for Implantable Devices, Birck Nanotechnology Center, Purdue University, West Lafayette, Indiana 47907, USA. ; School of Mechanical Engineering, Purdue University, West Lafayette, Indiana 47907, USA. ; Department of Mechanical Engineering, Civil and Environmental Engineering, Materials Science and Engineering, and Skin Disease Research Center, Northwestern University, Evanston, Illinois 60208, USA. ; Department of Biomedical Engineering, College of Health Science, Korea University, Seoul 136-703, South Korea. ; Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26779949" target="_blank"〉PubMed〈/a〉
    Keywords: *Absorbable Implants/adverse effects ; Administration, Cutaneous ; Animals ; Body Temperature ; Brain/*metabolism/surgery ; Electronics/*instrumentation ; Equipment Design ; Hydrolysis ; Male ; Monitoring, Physiologic/adverse effects/*instrumentation ; Organ Specificity ; Pressure ; *Prostheses and Implants/adverse effects ; Rats ; Rats, Inbred Lew ; *Silicon ; Telemetry/instrumentation ; Wireless Technology/instrumentation
    Print ISSN: 0028-0836
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    Policy: Urban physics (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pollock, Kevin -- England -- Nature. 2016 Mar 17;531(7594):S64-6. doi: 10.1038/531S64a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26981733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cities ; *City Planning ; Feedback ; Humans ; *Physics ; Plague/epidemiology ; Rats ; *Urbanization ; Vietnam/epidemiology
    Print ISSN: 0028-0836
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    A hippocampal network for spatial coding during immobility and sleep (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-05
    Description: How does an animal know where it is when it stops moving? Hippocampal place cells fire at discrete locations as subjects traverse space, thereby providing an explicit neural code for current location during locomotion. In contrast, during awake immobility, the hippocampus is thought to be dominated by neural firing representing past and possible future experience. The question of whether and how the hippocampus constructs a representation of current location in the absence of locomotion has been unresolved. Here we report that a distinct population of hippocampal neurons, located in the CA2 subregion, signals current location during immobility, and does so in association with a previously unidentified hippocampus-wide network pattern. In addition, signalling of location persists into brief periods of desynchronization prevalent in slow-wave sleep. The hippocampus thus generates a distinct representation of current location during immobility, pointing to mnemonic processing specific to experience occurring in the absence of locomotion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kay, Kenneth -- Sosa, Marielena -- Chung, Jason E -- Karlsson, Mattias P -- Larkin, Margaret C -- Frank, Loren M -- R01 MH090188/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 10;531(7593):185-90. doi: 10.1038/nature17144. Epub 2016 Mar 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UCSF Center for Integrative Neuroscience and Department of Physiology, University of California San Francisco, California 94158, USA. ; Howard Hughes Medical Institute, University of California San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934224" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Hippocampus/anatomy & histology/*cytology/*physiology ; Male ; Models, Neurological ; Movement ; Neurons/*physiology ; Orientation/*physiology ; Rats ; Rats, Long-Evans ; Sleep/*physiology ; Space Perception/*physiology ; Spatial Memory/physiology
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    Ageing: Restoration project (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGilvray, Annabel -- England -- Nature. 2016 Mar 3;531(7592):S4-5. doi: 10.1038/531S4a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934524" target="_blank"〉PubMed〈/a〉
    Keywords: Acetates/pharmacology/therapeutic use ; Aging/blood/drug effects/pathology/*psychology ; Alzheimer Disease/blood/therapy ; Animals ; Anti-Asthmatic Agents/pharmacology/therapeutic use ; Cognition Disorders/pathology/physiopathology/*prevention & control/*therapy ; Estrogens/pharmacology ; Female ; Hippocampus/drug effects/pathology/physiology/physiopathology ; Humans ; Inflammation Mediators/immunology ; Leukotrienes/immunology ; Macaca mulatta ; Male ; Mice ; Neuronal Plasticity/drug effects ; Parkinson Disease/therapy ; Plasma/chemistry/physiology ; Prefrontal Cortex/drug effects/pathology/physiology/physiopathology ; Quinolines/pharmacology/therapeutic use ; Rats ; Rejuvenation/*physiology/*psychology ; Synapses/drug effects/metabolism/pathology
    Print ISSN: 0028-0836
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    Neurobiology: Rise of resilience (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, Anthony -- England -- Nature. 2016 Mar 3;531(7592):S18-9. doi: 10.1038/531S18a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934522" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/metabolism ; Animals ; Brain/*physiology ; Bullying ; DNA Methylation ; Depression/complications/prevention & control/therapy ; Emotional Adjustment ; Epigenesis, Genetic/genetics ; Female ; Hippocampus/metabolism ; Humans ; Hydrocortisone/metabolism ; Maternal Behavior ; Memory/physiology ; Mice ; Models, Animal ; Oxytocin/metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects/genetics ; Psychological Trauma/complications/genetics/metabolism ; Rats ; *Resilience, Psychological ; Social Isolation/psychology ; Stress, Psychological/complications/genetics/metabolism/therapy
    Print ISSN: 0028-0836
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    Proton-gated Ca(2+)-permeable TRP channels damage myelin in conditions mimicking ischaemia (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-01-14
    Description: The myelin sheaths wrapped around axons by oligodendrocytes are crucial for brain function. In ischaemia myelin is damaged in a Ca(2+)-dependent manner, abolishing action potential propagation. This has been attributed to glutamate release activating Ca(2+)-permeable N-methyl-D-aspartate (NMDA) receptors. Surprisingly, we now show that NMDA does not raise the intracellular Ca(2+) concentration ([Ca(2+)]i) in mature oligodendrocytes and that, although ischaemia evokes a glutamate-triggered membrane current, this is generated by a rise of extracellular [K(+)] and decrease of membrane K(+) conductance. Nevertheless, ischaemia raises oligodendrocyte [Ca(2+)]i, [Mg(2+)]i and [H(+)]i, and buffering intracellular pH reduces the [Ca(2+)]i and [Mg(2+)]i increases, showing that these are evoked by the rise of [H(+)]i. The H(+)-gated [Ca(2+)]i elevation is mediated by channels with characteristics of TRPA1, being inhibited by ruthenium red, isopentenyl pyrophosphate, HC-030031, A967079 or TRPA1 knockout. TRPA1 block reduces myelin damage in ischaemia. These data suggest that TRPA1-containing ion channels could be a therapeutic target in white matter ischaemia.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4733665/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4733665/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamilton, Nicola B -- Kolodziejczyk, Karolina -- Kougioumtzidou, Eleni -- Attwell, David -- Wellcome Trust/United Kingdom -- England -- Nature. 2016 Jan 28;529(7587):523-7. doi: 10.1038/nature16519. Epub 2016 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Physiology &Pharmacology, University College London, Gower St., London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26760212" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Ischemia/*metabolism/*pathology ; Calcium/*metabolism ; Calcium Signaling/drug effects ; Electric Conductivity ; Female ; Hydrogen-Ion Concentration ; Magnesium/metabolism ; Male ; Mice ; Mice, Transgenic ; Multiple Sclerosis/metabolism/pathology ; Myelin Sheath/drug effects/*metabolism/*pathology ; N-Methylaspartate/metabolism/pharmacology ; Oligodendroglia/drug effects/metabolism/pathology ; Potassium/metabolism ; *Protons ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Stroke/metabolism/pathology ; Transient Receptor Potential Channels/antagonists & ; inhibitors/deficiency/genetics/*metabolism ; White Matter/metabolism/pathology
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    Smart drugs: A dose of intelligence (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dance, Amber -- England -- Nature. 2016 Mar 3;531(7592):S2-3. doi: 10.1038/531S2a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26934523" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Amphetamines/adverse effects/pharmacology ; Animals ; Benzhydryl Compounds/pharmacology ; Biomedical Enhancement/ethics/*methods ; Caffeine/pharmacology ; Child ; Cognition/drug effects ; Dopamine/metabolism ; Healthy Volunteers ; Humans ; Intelligence/*drug effects ; Intelligence Tests ; Methylphenidate/adverse effects/pharmacology ; Neurotransmitter Agents/metabolism ; Nicotine/adverse effects/pharmacology ; Norepinephrine/metabolism ; Off-Label Use ; Performance-Enhancing Substances/adverse effects/*pharmacology ; Prefrontal Cortex/drug effects/physiology ; Rats ; Substance-Related Disorders/etiology ; Video Games/psychology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    The conformational signature of beta-arrestin2 predicts its trafficking and signalling functions (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-24
    Description: Arrestins are cytosolic proteins that regulate G-protein-coupled receptor (GPCR) desensitization, internalization, trafficking and signalling. Arrestin recruitment uncouples GPCRs from heterotrimeric G proteins, and targets the proteins for internalization via clathrin-coated pits. Arrestins also function as ligand-regulated scaffolds that recruit multiple non-G-protein effectors into GPCR-based 'signalsomes'. Although the dominant function(s) of arrestins vary between receptors, the mechanism whereby different GPCRs specify these divergent functions is unclear. Using a panel of intramolecular fluorescein arsenical hairpin (FlAsH) bioluminescence resonance energy transfer (BRET) reporters to monitor conformational changes in beta-arrestin2, here we show that GPCRs impose distinctive arrestin 'conformational signatures' that reflect the stability of the receptor-arrestin complex and role of beta-arrestin2 in activating or dampening downstream signalling events. The predictive value of these signatures extends to structurally distinct ligands activating the same GPCR, such that the innate properties of the ligand are reflected as changes in beta-arrestin2 conformation. Our findings demonstrate that information about ligand-receptor conformation is encoded within the population average beta-arrestin2 conformation, and provide insight into how different GPCRs can use a common effector for different purposes. This approach may have application in the characterization and development of functionally selective GPCR ligands and in identifying factors that dictate arrestin conformation and function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Mi-Hye -- Appleton, Kathryn M -- Strungs, Erik G -- Kwon, Joshua Y -- Morinelli, Thomas A -- Peterson, Yuri K -- Laporte, Stephane A -- Luttrell, Louis M -- DK055524/DK/NIDDK NIH HHS/ -- GM095497/GM/NIGMS NIH HHS/ -- MOP-74603/Canadian Institutes of Health Research/Canada -- R01 DK055524/DK/NIDDK NIH HHS/ -- R01 GM095497/GM/NIGMS NIH HHS/ -- RR027777/RR/NCRR NIH HHS/ -- S10 RR027777/RR/NCRR NIH HHS/ -- England -- Nature. 2016 Mar 31;531(7596):665-8. doi: 10.1038/nature17154. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Medical University of South Carolina, Charleston, South Carolina 29425, USA. ; Department of Pharmaceutical &Biomedical Sciences, College of Pharmacy, Medical University of South Carolina, Charleston, South Carolina 29425, USA. ; Department of Medicine, McGill University Health Center Research Institute, McGill University, Quebec H4A 3J1, Canada. ; Pharmacology and Therapeutics, McGill University, Quebec H3G 1Y6, Canada. ; Anatomy and Cell Biology, McGill University, Quebec H3A 0C7, Canada. ; Research Service of the Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29401, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arrestins/*chemistry/*metabolism ; Enzyme Activation ; HEK293 Cells ; Humans ; Ligands ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Protein Conformation ; Protein Transport ; Rats ; Receptors, G-Protein-Coupled/chemistry/*metabolism ; *Signal Transduction
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    Effector T-cell trafficking between the leptomeninges and the cerebrospinal fluid (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-02-11
    Description: In multiple sclerosis, brain-reactive T cells invade the central nervous system (CNS) and induce a self-destructive inflammatory process. T-cell infiltrates are not only found within the parenchyma and the meninges, but also in the cerebrospinal fluid (CSF) that bathes the entire CNS tissue. How the T cells reach the CSF, their functionality, and whether they traffic between the CSF and other CNS compartments remains hypothetical. Here we show that effector T cells enter the CSF from the leptomeninges during Lewis rat experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. While moving through the three-dimensional leptomeningeal network of collagen fibres in a random Brownian walk, T cells were flushed from the surface by the flow of the CSF. The detached cells displayed significantly lower activation levels compared to T cells from the leptomeninges and CNS parenchyma. However, they did not represent a specialized non-pathogenic cellular sub-fraction, as their gene expression profile strongly resembled that of tissue-derived T cells and they fully retained their encephalitogenic potential. T-cell detachment from the leptomeninges was counteracted by integrins VLA-4 and LFA-1 binding to their respective ligands produced by resident macrophages. Chemokine signalling via CCR5/CXCR3 and antigenic stimulation of T cells in contact with the leptomeningeal macrophages enforced their adhesiveness. T cells floating in the CSF were able to reattach to the leptomeninges through steps reminiscent of vascular adhesion in CNS blood vessels, and invade the parenchyma. The molecular/cellular conditions for T-cell reattachment were the same as the requirements for detachment from the leptomeningeal milieu. Our data indicate that the leptomeninges represent a checkpoint at which activated T cells are licensed to enter the CNS parenchyma and non-activated T cells are preferentially released into the CSF, from where they can reach areas of antigen availability and tissue damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schlager, Christian -- Korner, Henrike -- Krueger, Martin -- Vidoli, Stefano -- Haberl, Michael -- Mielke, Dorothee -- Brylla, Elke -- Issekutz, Thomas -- Cabanas, Carlos -- Nelson, Peter J -- Ziemssen, Tjalf -- Rohde, Veit -- Bechmann, Ingo -- Lodygin, Dmitri -- Odoardi, Francesca -- Flugel, Alexander -- England -- Nature. 2016 Feb 18;530(7590):349-53. doi: 10.1038/nature16939. Epub 2016 Feb 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuroimmunology, Institute for Multiple Sclerosis Research, University Medical Centre Gottingen, 37073 Gottingen, Germany. ; Institute of Anatomy, University of Leipzig, 04103 Leipzig, Germany. ; Department of Structural and Geotechnical Engineering, University of Rome La Sapienza, 00185 Rome, Italy. ; Department Neurosurgery, University Medical Centre Gottingen, 37075 Gottingen, Germany. ; Division of Immunology, Department of Pediatrics Dalhousie University, Halifax B3H 4R2, Canada. ; Departamento de Biologia Celular e Inmunologia, Centro de Biologia Molecular Severo Ochoa, 28049 Madrid, Spain. ; Medical Clinic and Policlinic IV, Ludwig-Maximilians-University of Munich, 80336 Munich, Germany. ; Department of Neurology, University Hospital, 01307 Dresden, Germany. ; Max-Planck-Institute for Experimental Medicine, 37075 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26863192" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; Cell Adhesion ; *Cell Movement ; Cerebrospinal Fluid/*cytology/immunology ; Chemokines/metabolism ; Choroid Plexus ; Collagen/metabolism ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/immunology/*pathology ; Female ; Integrin alpha4beta1/metabolism ; Lymphocyte Activation ; Lymphocyte Function-Associated Antigen-1/metabolism ; Macrophages/immunology/metabolism ; Male ; Meninges/immunology/*pathology ; Multiple Sclerosis/immunology/*pathology ; Rats ; Rats, Inbred Lew ; Receptors, CCR5/metabolism ; Receptors, CXCR3/metabolism ; T-Lymphocytes/immunology/*pathology
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    The peptidergic control circuit for sighing (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-02-09
    Description: Sighs are long, deep breaths expressing sadness, relief or exhaustion. Sighs also occur spontaneously every few minutes to reinflate alveoli, and sighing increases under hypoxia, stress, and certain psychiatric conditions. Here we use molecular, genetic, and pharmacologic approaches to identify a peptidergic sigh control circuit in murine brain. Small neural subpopulations in a key breathing control centre, the retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG), express bombesin-like neuropeptide genes neuromedin B (Nmb) or gastrin-releasing peptide (Grp). These project to the preBotzinger Complex (preBotC), the respiratory rhythm generator, which expresses NMB and GRP receptors in overlapping subsets of ~200 neurons. Introducing either neuropeptide into preBotC or onto preBotC slices, induced sighing or in vitro sigh activity, whereas elimination or inhibition of either receptor reduced basal sighing, and inhibition of both abolished it. Ablating receptor-expressing neurons eliminated basal and hypoxia-induced sighing, but left breathing otherwise intact initially. We propose that these overlapping peptidergic pathways comprise the core of a sigh control circuit that integrates physiological and perhaps emotional input to transform normal breaths into sighs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Peng -- Janczewski, Wiktor A -- Yackle, Kevin -- Kam, Kaiwen -- Pagliardini, Silvia -- Krasnow, Mark A -- Feldman, Jack L -- HL40959/HL/NHLBI NIH HHS/ -- HL70029/HL/NHLBI NIH HHS/ -- NS72211/NS/NINDS NIH HHS/ -- R01 HL040959/HL/NHLBI NIH HHS/ -- R01 HL070029/HL/NHLBI NIH HHS/ -- R01 NS072211/NS/NINDS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Feb 18;530(7590):293-7. doi: 10.1038/nature16964. Epub 2016 Feb 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, California 94305, USA. ; Systems Neurobiology Laboratory, Department of Neurobiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26855425" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bombesin/pharmacology ; Emotions/physiology ; Female ; Gastrin-Releasing Peptide/deficiency/genetics/*metabolism ; In Vitro Techniques ; Male ; Mice ; Mice, Inbred C57BL ; Neurokinin B/*analogs & derivatives/deficiency/genetics/metabolism/pharmacology ; Neurons/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Bombesin/*metabolism ; *Respiration/drug effects ; Respiratory Center/cytology/drug effects/physiology ; Ribosome Inactivating Proteins, Type 1/pharmacology ; Signal Transduction/drug effects/*physiology
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    A prefrontal-thalamo-hippocampal circuit for goal-directed spatial navigation (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-05-29
    Description: Spatial navigation requires information about the relationship between current and future positions. The activity of hippocampal neurons appears to reflect such a relationship, representing not only instantaneous position but also the path towards a goal location. However, how the hippocampus obtains information about goal direction is poorly understood. Here we report a prefrontal-thalamic neural circuit that is required for hippocampal representation of routes or trajectories through the environment. Trajectory-dependent firing was observed in medial prefrontal cortex, the nucleus reuniens of the thalamus, and the CA1 region of the hippocampus in rats. Lesioning or optogenetic silencing of the nucleus reuniens substantially reduced trajectory-dependent CA1 firing. Trajectory-dependent activity was almost absent in CA3, which does not receive nucleus reuniens input. The data suggest that projections from medial prefrontal cortex, via the nucleus reuniens, are crucial for representation of the future path during goal-directed behaviour and point to the thalamus as a key node in networks for long-range communication between cortical regions involved in navigation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Hiroshi T -- Zhang, Sheng-Jia -- Witter, Menno P -- Moser, Edvard I -- Moser, May-Britt -- England -- Nature. 2015 Jun 4;522(7554):50-5. doi: 10.1038/nature14396. Epub 2015 May 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kavli Institute for Systems Neuroscience and Centre for Neural Computation, Norwegian University of Science and Technology, Olav Kyrres gate 9, MTFS, 7491 Trondheim, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26017312" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; CA1 Region, Hippocampal/cytology/*physiology ; CA3 Region, Hippocampal/cytology/physiology ; *Goals ; Male ; Maze Learning ; Midline Thalamic Nuclei/cytology/physiology ; Neural Pathways/*physiology ; Neurons/physiology ; Optogenetics ; Prefrontal Cortex/cytology/*physiology ; Rats ; Rats, Long-Evans ; Spatial Navigation/*physiology ; Thalamus/cytology/*physiology
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    Immunofluorescence of NADPH-cytochrome c (P-450) reductase in rat and minipig tissues injected with phenobarbital (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-06-27
    Description: The enzyme NADPH-cytochrome c (P-450) reductase was identified by indirect immunofluorescence in hepatocytes, bronchioles, and proximal tubules of liver, lung, and kidney, respectively, of rats and minipigs that had been injected with phenobarbital or saline. The distribution of this component of the cytochrome P-450-mediated microsomal system may be relevant to sites of drug toxicity and carcinogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dees, J H -- Coe, L D -- Yasukochi, Y -- Masters, B S -- New York, N.Y. -- Science. 1980 Jun 27;208(4451):1473-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6770464" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Fluorescent Antibody Technique ; Kidney/drug effects/*enzymology ; Liver/drug effects/*enzymology ; Lung/drug effects/*enzymology ; Male ; NADPH-Ferrihemoprotein Reductase/*metabolism ; Organ Specificity ; Phenobarbital/*pharmacology ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    L-Ornithine decarboxylase:an essential role in early mammalian embryogenesis (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-05-02
    Description: The highly selective, enzyme-activated, irreversible inhibitor of L-ornithine decarboxylase, DL-alpha-difluoromethylornithine, suppresses the increase in uterine L-ornithine decarboxylase activity associated with early embryogenesis in the mouse and arrests embryonic development at that stage. Contragestational effects were confirmed in the rat and rabbit. An increase in L-ornithine decarboxylase activity that leads to a rapid increase in putrescine concentration appears to be essential during a critical period after implantation for continued mammalian embryonal growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fozard, J R -- Part, M L -- Prakash, N J -- Grove, J -- Schechter, P J -- Sjoerdsma, A -- Koch-Weser, J -- New York, N.Y. -- Science. 1980 May 2;208(4443):505-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6768132" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosylmethionine Decarboxylase/metabolism ; Animals ; Carboxy-Lyases/*physiology ; Eflornithine ; Embryo, Mammalian/drug effects/*physiology ; Female ; Gestational Age ; Mice ; Ornithine/*analogs & derivatives/pharmacology ; Ornithine Decarboxylase/*physiology ; Ornithine Decarboxylase Inhibitors ; Polyamines/metabolism ; Pregnancy ; Rabbits ; Rats ; Uterus/drug effects/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Bioactive conformation of luteinizing hormone-releasing hormone: evidence from a conformationally constrained analog (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-11-07
    Description: An analog of luteinizing hormone-releasing hormone containing a gamma-lactam as a conformational constraint has been prepared with the use of a novel cyclization of a methionine sulfonium salt. The analog is more active as a luteinizing hormone-releasing hormone agonist that the parent hormone, and provides evidence for a bioactive conformation containing a beta-turn.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freidinger, R M -- Veber, D F -- Perlow, D S -- Brooks, J R -- Saperstein, R -- New York, N.Y. -- Science. 1980 Nov 7;210(4470):656-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7001627" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Assay ; Cells, Cultured ; Female ; *Gonadotropin-Releasing Hormone/analogs & derivatives ; Hydrogen Bonding ; Lactams ; Protein Conformation ; Rats ; Structure-Activity Relationship
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    Reorganization of the axon membrane in demyelinated peripheral nerve fibers: morphological evidence (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-11-07
    Description: Cytochemical staining of demyelinated peripheral axons revealed two types of axon membrane organization, one of which suggests that the demyelinated axolemma acquires a high density of sodium channels. Ferric ion-ferrocyanide stain was confined to a restricted region of axon membrane at the beginning of a demyelinated segment or was distributed throughout the demyelinated segment of axon. The latter pattern represents one possible morphological correlate of continuous conduction through a demyelinated segment and suggests a reorganization of the axolemma after demyelination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Foster, R E -- Whalen, C C -- Waxman, S G -- NS-15320/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1980 Nov 7;210(4470):661-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6159685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Demyelinating Diseases/metabolism/*pathology ; Disease Models, Animal ; Ion Channels/*metabolism ; Male ; Neural Conduction ; Neurilemma/*metabolism/pathology ; Rats ; Staining and Labeling
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    Doridosine: a new hypotensive N-methylpurine riboside from the nudibranch Anisodoris nobilis (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-01-11
    Description: A new N-methylpurine riboside (doridosine), probably N1-Methylisoguanosine, was isolated from the digestive glands of a nudibranch. Doridosine produces prolonged hypotension and bradycardia in anesthetized rats, decreases the rate and the amplitude of contraction of guinea pig atria in vitro, and causes the heart rate in anesthetized mice to be reduced by 50 percent for many hours after which the animals recover completely.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fuhrman, F A -- Fuhrman, G J -- Kim, Y H -- Pavelka, L A -- Mosher, H S -- New York, N.Y. -- Science. 1980 Jan 11;207(4427):193-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7350655" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antihypertensive Agents/*isolation & purification ; Guanosine/*analogs & derivatives/isolation & purification/pharmacology ; Guinea Pigs ; Heart Rate/drug effects ; Mice ; Mollusca/analysis ; Rats
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    DNA polymerases in parasitic protozoans differ from host enzymes (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-05-02
    Description: Analysis of extracts of the bloodstream forms of Trypanosoma brucei showed that both DNA polymerase-alpha and DNA polymerase-beta activities were present. The detection of DNA polymerase-beta in T. brucei demonstrates the presence of this enzyme in unicellular organisms. DNA polymerase-beta is present also in Leishmania mexicana. The DNA polymerases in T. brucei are immunologically distinct from the host enzymes. The structural differences between the parasite and the host enzymes could be exploited for the development of agents to combat parasitic diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, L M -- Cheriathundam, E -- Mahoney, E M -- Cerami, A -- New York, N.Y. -- Science. 1980 May 2;208(4443):510-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7367875" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Centrifugation, Density Gradient ; Chickens ; DNA Polymerase I/analysis ; DNA Polymerase II/analysis ; DNA Polymerase III/analysis ; DNA-Directed DNA Polymerase/*analysis ; Fishes ; Immune Sera ; Leishmania/*enzymology ; Molecular Weight ; Rabbits ; Rats ; Species Specificity ; Trypanosoma brucei brucei/*enzymology
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    Oral contraceptives, lanosterol, and platelet hyperactivity in rat (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-11-07
    Description: Lanosterol, a cholesterol precursor that increases considerably in the platelets of rats treated with oral contraceptives, was incubated with either platelet-rich plasma or washed platelet suspension. After 2 minutes there was a remarkable dose-related increase in platelet activity. This platelet hyperactivity was measured by clotting time and platelet aggregation could not be reproduced by cholesterol or ethinylestradiol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ciavatti, M -- Dumont, E -- Benoit, C -- Renaud, S -- New York, N.Y. -- Science. 1980 Nov 7;210(4470):642-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7433990" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Coagulation/*drug effects ; Blood Platelets/*drug effects ; Contraceptives, Oral/*pharmacology ; Dose-Response Relationship, Drug ; Female ; Lanosterol/*pharmacology ; Platelet Aggregation/*drug effects ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Neurochemical and behavioral evidence for a selective presynaptic dopamine receptor agonist (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-12-05
    Description: A new dopamine analog, 6,7-dihydroxy-2-dimethylaminotetralin (TL-99), was compared to apomorphine in three tests of dopaminergic function in the central nervous system. The tests, performed on rats, included production of changes in locomotor activity (involving both presynaptic and postsynaptic receptors), inhibition of dopa accumulation (quantifying presynaptic receptor activity), and the rotation model (quantifying postsynaptic receptor activation). Apomorphine was efficacious at both presynaptic and postsynaptic receptors, whereas TL-99 was much more efficacious at the presynaptic receptor. This result indicates not only that differences exist between presynaptic and postsynaptic dopamine receptors, but also that these differences may be exploited in the design of selective dopamine agonists.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodale, D P -- Rusterholz, D B -- Long, J P -- Flynn, J R -- Walsh, B -- Cannon, J G -- Lee, T -- GM 12675/GM/NIGMS NIH HHS/ -- GM-22365/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1980 Dec 5;210(4474):1141-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7444443" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apomorphine/pharmacology ; Behavior, Animal/drug effects ; Brain/*drug effects ; Levodopa/metabolism ; Motor Activity/drug effects ; Naphthols ; Rats ; Receptors, Dopamine/*drug effects ; Synaptic Membranes/*drug effects ; *Tetrahydronaphthalenes
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    Phospholipid methylation and biological signal transmission (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-09-05
    Description: Many types of cells methylate phospholipids using two methyltransferase enzymes that are asymmetrically distributed in membranes. As the phospholipids are successively methylated, they are translocated from the inside to the outside of the membrane. When catecholamine neurotransmitters, lectins, immunoglobulins or chemotaxic peptides bind to the cell surface, they stimulate the methyltransferase enzymes and reduce membrane viscosity. The methylation of phospholipids is coupled to Ca2+ influx and the release of arachidonic acid, lysophosphatidylcholine, and prostaglandins. These closely associated biochemical changes facilitate the transmission of many signals through membranes, resulting in the generation of adenosine 3',5'-monophophate in many cell types, release of histamine in mast cells and basophils, mitogenesis in lymphocytes, and chemotaxis in neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirata, F -- Axelrod, J -- New York, N.Y. -- Science. 1980 Sep 5;209(4461):1082-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6157192" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/metabolism ; Animals ; Arachidonic Acids/metabolism ; Calcium/metabolism ; Cell Membrane/metabolism ; Chemotaxis, Leukocyte ; Histamine Release ; Lymphocyte Activation ; *Membrane Fluidity ; Membrane Lipids/*metabolism ; Methylation ; Phosphatidylcholines/metabolism ; Phosphatidylethanolamines/metabolism ; Phospholipids/*metabolism ; Rats ; Receptors, Adrenergic, beta/metabolism ; Receptors, Drug/*physiology ; S-Adenosylmethionine/metabolism
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    Antibodies to cerebroside sulfate inhibit the effects of morphine and beta-endorphin (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-01-04
    Description: Morphine and beta-endorphin inhibit the shaking response of pentobarbital-anesthetized rats to ice water. Stereotaxically guided administration of antibodies to cerebroside sulfate into the periaqueductal gray region, the most sensitive brain region in which to demonstrate inhibition of this response, antagonizes the effect of morphine and beta-endorphin. These results suggest that cerebroside sulfate may be an integral component of an opiate receptor in rat brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Craves, F B -- Zalc, B -- Leybin, L -- Baumann, N -- Loh, H H -- New York, N.Y. -- Science. 1980 Jan 4;207(4426):75-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6243189" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Reactions ; Behavior, Animal/drug effects ; Biological Assay ; Brain/*immunology ; Cerebral Aqueduct ; Endorphins/*antagonists & inhibitors ; Male ; Morphine/*antagonists & inhibitors ; Pentobarbital/pharmacology ; Rats ; Receptors, Opioid/*immunology ; Sulfoglycosphingolipids/*immunology
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    Photosynthesis of previtamin D3 in human skin and the physiologic consequences (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-10-10
    Description: Photosynthesis of previtamin D3 can occur throughout the epidermis in the dermis when hypopigmented Caucasian skin is exposed to solar ultraviolet radiation. Once previtamin D3 is formed in the skin, it undergoes a temperature-dependent thermal isomerization that takes at least 3 days to complete. The vitamin D-binding protein preferentially translocates the thermal product, vitamin D3, into the circulation. These processes suggest a unique mechanism for the synthesis, storage, and slow, steady release of vitamin D3 from the skin into the circulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holick, M F -- MacLaughlin, J A -- Clark, M B -- Holick, S A -- Potts, J T Jr -- Anderson, R R -- Blank, I H -- Parrish, J A -- Elias, P -- AM25395-01/AM/NIADDK NIH HHS/ -- AM27334-01/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1980 Oct 10;210(4466):203-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6251551" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/metabolism ; Cholecalciferol/*biosynthesis ; Cholestadienols/*biosynthesis ; Dose-Response Relationship, Radiation ; Hot Temperature ; Humans ; Isomerism ; Photochemistry ; Rats ; Skin/cytology/*metabolism ; Ultraviolet Rays ; Vitamin D/metabolism ; Vitamin D-Binding Protein
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  • 79
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    Excitatory and inhibitory effects of opiates in the rat vas deferens: a dual mechanism of opiate action (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-10-03
    Description: Both natural (-)-morphine and its unnatural enantiomer (+)-morphine exert an excitatory action on electrically stimulated contractions of rat vas deferens. Preexposure to (-)-morphine results in cross-tolerance to the inhibitory action of beta-endorphin. (-)-Naloxone and its stereoisomer (+)-naloxone also exert an excitatory action, but only (-)-naloxone bocks the inhibtory action of beta-endorphin. Thus morphine exerts a dual action on a peripheral organ: one an inhibitory action mediated by the stereospecific endorphin receptor that is blocked stereospecifically by naloxone, the other an excitatory action mediated by a nonstereospecific receptor that is not blocked by naloxone. The opiate abstinence syndrome is seen as due to the unmasking of the excitatory action of opiates when its concomitant inhibitory influence is removed by selective blockade by naloxone or weakened by selective tolerance. The view that the rat vas deferens is devoid of morphine receptors is now seen as arising from a reverse example of morphine's dual action: the masking of the inhibitory action of morphine by its concomitant and more potent excitatory action.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacquet, Y F -- DA 00367/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1980 Oct 3;210(4465):95-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6158098" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drug Interactions ; Endorphins/pharmacology ; Male ; Morphine/antagonists & inhibitors/pharmacology ; Muscle Contraction/drug effects ; Naloxone/pharmacology ; Narcotics/*pharmacology ; Rats ; Receptors, Opioid/drug effects ; Stereoisomerism ; Substance P/pharmacology ; Vas Deferens/*drug effects
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  • 80
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    Insulin receptors: differences in structural organization on adipocyte and liver plasma membranes (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-12-05
    Description: Comparison was made of the distribution of the insulin receptor sites on adipocyte and liver plasma membranes by using ferritin-insulin. Two-thirds of the occupied insulin receptors on adipocytes occurred in groups of two or more whereas up to two-thirds of the receptors on liver occurred as single receptors. Ferritin-insulin did not cause aggregation of the receptor sites in either tissue. The naturally occurring groups of receptors on adipocyte membranes may play a role in the greater sensitivity of adipocytes to insulin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jarett, L -- Schweitzer, J B -- Smith, R M -- AM 20097/AM/NIADDK NIH HHS/ -- T32 AM 07296/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1980 Dec 5;210(4474):1127-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7003710" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*ultrastructure ; Animals ; Cell Membrane/ultrastructure ; Insulin/metabolism ; Liver/*ultrastructure ; Macromolecular Substances ; Membrane Fluidity ; Oxidation-Reduction ; Protein Binding ; Rats ; *Receptor, Insulin/metabolism ; Sulfhydryl Compounds
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  • 81
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    Dorsal root ganglion neurons are destroyed by exposure in utero to maternal antibody to nerve growth factor (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-11-21
    Description: Rats and guinea pigs, when immunized with mouse nerve growth factor, produce antibodies that cross-react with their own nerve growth factor. The antibodies reach developing offspring of these animals both prenatally (rats and guinea pigs) and postnatally (rats). Depriving the fetus of nerve growth factor in this way results in the destruction of up to 85 percent of dorsal root ganglion neurons as well as destruction of sympathetic neurons. Sensory neurons of placodal origin in the nodose ganglion were not affected. These data demonstrate that dorsal root ganglion neurons go through a phase of nerve growth factor dependence in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, E M Jr -- Gorin, P D -- Brandeis, L D -- Pearson, J -- HD12260/HD/NICHD NIH HHS/ -- HL20604/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1980 Nov 21;210(4472):916-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7192014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies ; Female ; Ganglia, Spinal/cytology/*embryology/growth & development ; Guinea Pigs ; Lactation ; Maternal-Fetal Exchange ; Milk/immunology ; Nerve Growth Factors/*immunology ; Pregnancy ; Rats
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  • 82
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    Maternal glucocorticoid hormones influence neurotransmitter phenotypic expression in embryos (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-10-31
    Description: Treatment of pregnant rats with reserpine prevented the normal disappearance of catecholamine fluorescence in presumptive neuroblasts of the embryonic gut. These cells normally express the noradrenergic phenotype transiently during embryonic development. The effect of reserpine was reproduced by treating mothers with hydrocortisone acetate. Moreover, the reserpine effect was blocked by treatment with dexamethasone, which inhibits the stress-induced increase in plasma glucocorticoids, and by mitotone, which causes adrenocortical cytolysis. It is concluded that reserpine, through the mediation of maternal glucocorticoid hormones, alters the phenotypic expression of these embryonic neuroblasts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jonakait, G M -- Bohn, M C -- Black, I B -- HD 12108/HD/NICHD NIH HHS/ -- NS 06400/NS/NINDS NIH HHS/ -- NS 10259/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1980 Oct 31;210(4469):551-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7423206" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catecholamines/metabolism ; Female ; Hydrocortisone/*pharmacology ; Intestines/*embryology/innervation ; Maternal-Fetal Exchange ; Pregnancy ; Pregnancy, Animal/*drug effects ; Rats ; Reserpine/*pharmacology ; Sympathetic Nervous System/*embryology
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  • 83
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    Visualization of specific angiotensin II binding sites in the brain by fluorescent microscopy (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-11-14
    Description: The organum vasculosum of the lamina terminalis has been implicated as the site of receptors mediating central responses of angiotensin II. Up to now, this had been based on indirect evidence, but direct visualization of angiotensin II at its site of action has now been achieved by the use of a biologically active fluorescent angiotensin II agonist. The ventricular surface of the organum vasculosum lamina terminalis showed intense fluorescence, which was virtually eliminated by an excess of unlabeled angiotensin II.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Landas, S -- Phillips, M I -- Stamler, J F -- Raizada, M K -- AM25295/AM/NIADDK NIH HHS/ -- HL14388/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1980 Nov 14;210(4471):791-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6254147" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/*metabolism/physiology ; Animals ; Cerebral Ventricles/*metabolism ; Drinking Behavior/physiology ; Male ; Microscopy, Fluorescence ; Rats ; Receptors, Angiotensin/*metabolism ; Receptors, Cell Surface/*metabolism
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  • 84
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    Prolongation of islet xenograft survival without continuous immunosuppression (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-07-11
    Description: The survival of isolated rat islets transplanted into diabetic mice was prolonged markedly by maintaining the rat islets in vitro at 24 degrees C for 7 days before transplantation and administering to the recipients a single injection of antiserum to mouse and rat lymphocytes shortly before transplantation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lacy, P E -- Davie, J M -- Finke, E H -- New York, N.Y. -- Science. 1980 Jul 11;209(4453):283-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6770465" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/analysis ; Cell Survival ; Cells, Cultured ; Diabetes Mellitus, Experimental/*therapy ; *Immunosuppression ; *Islets of Langerhans Transplantation ; Lymphocytes/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Rats ; Transplantation, Heterologous ; Transplantation, Isogeneic
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  • 85
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    Microencapsulated islets as bioartificial endocrine pancreas (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-11-21
    Description: Single implantation of microencapsulated islets into rats with streptozotocin-induced diabetes corrected the diabetic state for 2 to 3 weeks. The microencapsulated islets remained morphologically and functionally intact throughout long-term culture studies lasting over 15 weeks.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, F -- Sun, A M -- New York, N.Y. -- Science. 1980 Nov 21;210(4472):908-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6776628" target="_blank"〉PubMed〈/a〉
    Keywords: Alginates/*therapeutic use ; Animals ; Cell Survival ; Diabetes Mellitus, Experimental/*therapy ; *Islets of Langerhans Transplantation ; Permeability ; Rats ; Transplantation, Homologous
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  • 86
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    Liver tumors induced in rats by oral administration of the antihistaminic methapyrilene hydrochloride (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-08-15
    Description: The antihistaminic over-the-counter drug methapyrilene hydrochloride, mixed with food at a concentration of 0.1 percent, was administered to 50 male and 50 female Fischer rats. A second group of 50 male and 50 female rats was given the same treatment together with 0.2 percent of sodium nitrite added to the food. Almost all of the rats in both groups developed liver neoplasms, mainly hepatocellular carcinomas and cholangiocarcinomas. The first rat died with a liver neoplasm at the 43rd week. Over 50 percent of the rats in both groups had metastases from the carcinomas of the liver to distant organs. Control rats treated with nitrite only, or untreated, did not develop liver neoplasms. There was no discernible effect of nitrite on the carcinogenicity of methapyrilene hydrochloride.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lijinsky, W -- Reuber, M D -- Blackwell, B N -- New York, N.Y. -- Science. 1980 Aug 15;209(4458):817-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7403848" target="_blank"〉PubMed〈/a〉
    Keywords: Aminopyridines/*toxicity ; Animals ; *Carcinogens ; Drug Interactions ; Female ; Liver Neoplasms, Experimental/*chemically induced/pathology ; Male ; Methapyrilene/*toxicity ; Neoplasm Metastasis ; Nitrites ; Rats
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    Mutagenic activity in photocopies (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-08-29
    Description: Extracts from several different photocopies were mutagenic in the Ames Salmonella assay. The mutagenic behavior was similar for extracts from copies and corresponding toners indicating that toners are directly responsible for the mutagenicity. The mutagenicity is caused by at least two classes of compounds which may be present either alone or in combination in any toner.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lofroth, G -- Hefner, E -- Alfheim, I -- Mooller, M -- New York, N.Y. -- Science. 1980 Aug 29;209(4460):1037-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6996094" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotransformation ; Carbon ; *Copying Processes ; Drug Evaluation, Preclinical/methods ; Microsomes, Liver/metabolism ; *Mutagens ; Photography ; Pyrenes/adverse effects ; Rats ; Salmonella typhimurium/drug effects
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  • 88
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    Sexual dimorphism in extent of axonal sprouting in rat hippocampus (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-06-13
    Description: Sympathetic axons, normally innervating the extracerebral vasculature, sprout into denervated regions of the hippocampal formation after lesions of the medial septal nucleus or fimbria in adult female rats. Similar lesions in adult males also elicit the sympathetic ingrowth; however, the number of anomalous axons is greatly reduced and their distribution is altered. In adult males the sympathetic axons do not send out collaterals within the stratum oriens of region CA3 or the molecular layer or deep hilar regions of the area dentata, as they do in adult females. Lesions in juveniles of both sexes result in more vigorous sprouting than in their adult counterparts. In the young males the anomalous axons are distributed more extensively into the dentate molecular layer; in the young females the axons merely send out more collaterals within the same regions as in the adults. This sexually dimorphic response to central nervous system damage suggests either that the sprouting is affected by the hormonal environment of the mature hippocampal system or that this brain region, like the hypothalamus, may express permanent morphological or physiological differences as a result of exposure to sex steroids during development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Loy, R -- Milner, T A -- New York, N.Y. -- Science. 1980 Jun 13;208(4449):1282-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7375941" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Axons/growth & development ; Denervation ; Female ; Gonadal Steroid Hormones/physiology ; Hippocampus/*cytology ; Male ; Neural Pathways/cytology ; Rats ; *Sex ; Sympathetic Nervous System/*cytology/growth & development
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  • 89
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    Ornithine decarboxylase is important in intestinal mucosal maturation and recovery from injury in rats (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-10-10
    Description: A transient increase in ornithine decarboxylase activity and polyamine biosynthesis occurs in the intestinal mucosa of the newborn rat in the third week after birth. During this period, there is a rapid conversion of the mucosa from a fetal to a mature adult status. A similar increase in ornithine decarboxylase activity also accompanies the rapid recovery of the mucosa 1 week after an injury is induced by chemotherapy in adult rats. In vivo, alpha-difluoromethyl ornithine, a highly selective, enzyme-activated, irreversible inhibitor, suppresses these increases in mucosal ornithine decarboxylase and delays both intestinal mucosal maturation and recovery from injury. Thus increased ornithine decarboxylase activity, with the resultant increase in polyamine content, may play an essential role in intestinal mucosal maturation and regeneration in the rat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lux, G D -- Marton, L J -- Baylin, S B -- 5-R01-18404/PHS HHS/ -- 5-T32-AM-07192-03/AM/NIADDK NIH HHS/ -- P50-HL-19157-01/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1980 Oct 10;210(4466):195-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6774420" target="_blank"〉PubMed〈/a〉
    Keywords: Amine Oxidase (Copper-Containing)/metabolism ; Animals ; Carboxy-Lyases/*physiology ; Cell Differentiation ; Cell Division ; Cytarabine/pharmacology ; Intestinal Mucosa/cytology/drug effects/*physiology ; Ornithine Decarboxylase/*physiology ; Ornithine Decarboxylase Inhibitors ; Putrescine/metabolism ; Rats ; Spermidine/metabolism ; Wound Healing
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  • 90
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    Phenacetin safety (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-01-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macklin, A W -- Welch, R M -- New York, N.Y. -- Science. 1980 Jan 11;207(4427):129-30, 132.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7350647" target="_blank"〉PubMed〈/a〉
    Keywords: Aminopyrine/adverse effects/toxicity ; Animals ; Humans ; Mice ; Mutagens ; Phenacetin/administration & dosage/*adverse effects/toxicity ; Rats
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  • 91
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    Local effect of the blastocyst on estrogen and progesterone receptors in the rat endometrium (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-03-07
    Description: Nuclear receptors for both estradiol and progesterone were present in twofold higher concentrations in implantation sites than in nonimplantation regions of the endometrium of 6-day pregnant rats. Decidualization in the absence of an embryo was not accompanied by a similar increase in the concentration of nuclear receptors. Moreover, this difference in receptor distribution between the implantation and nonimplantation areas persisted when a major part of the maternal supply of sex steroids was suppressed by ovariectomy on day 5 of pregnancy. These results support the hypothesis that steroids originating from the embryo affect the endometrial implantation site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Logeat, F -- Sartor, P -- Hai, M T -- Milgrom, E -- New York, N.Y. -- Science. 1980 Mar 7;207(4435):1083-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7355273" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*metabolism ; Castration ; Cell Nucleus/metabolism ; Decidua/metabolism ; Endometrium/*metabolism/ultrastructure ; Female ; Gestational Age ; Pregnancy ; Pseudopregnancy ; Rats ; Receptors, Estrogen/*metabolism ; Receptors, Progesterone/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    Retina-dependent activation by apomorphine of metabolic activity in the superficial layer of the superior colliculus (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-01-18
    Description: Studies of the effect of the dopamine agonist apomorphine on local cerebral glucose utilization by means of the carbon-14-labeled deoxyglucose method demonstrate a dose-dependent metabolic activation in the superficial layer of the superior colliculus in the rat. Apomorphine stimulated glucose utilization in a number of other cerebral structures, but only the effect in the superficial layer of the superior colliculus depended on an intact retinal input. This effect was present with the animal in the light or in the dark, but was abolished by enucleation, which left the effects in other cerebral structures unimpaired. Activation of the superificial layer of the superior colliculus appears, therefore, to be secondary to an action of apomorphine on dopaminergic systems within the retina.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCulloch, J -- Savaki, H E -- McCulloch, M C -- Sokoloff, L -- New York, N.Y. -- Science. 1980 Jan 18;207(4428):313-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7350662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apomorphine/*pharmacology ; Dark Adaptation ; Dopamine/*physiology ; Functional Laterality ; Geniculate Bodies/metabolism ; Glucose/*metabolism ; Rats ; Retina/*physiology ; Superior Colliculi/drug effects/*metabolism ; Visual Cortex/metabolism ; Visual Pathways/physiology ; Visual Perception/*physiology
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  • 93
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    Blue light and bilirubin excretion (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-04-11
    Description: Blue light converts bilirubin in the skin of jaundiced rats to metastable geometric isomers that are transported in blood and excreted in bile. The same reaction probably occurs in jaundiced babies exposed to light, particularly during treatment with phototherapy. Excretion of unisomerized bilirubin is prevented by intramolecular hydrogen bonding, and the pigment has to be metabolized to more polar derivatives to be excreted efficiently.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonagh, A F -- Palma, L A -- Lightner, D A -- New York, N.Y. -- Science. 1980 Apr 11;208(4440):145-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7361112" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile/analysis ; Bilirubin/*blood/metabolism ; Humans ; Infant, Newborn ; Jaundice, Neonatal/therapy ; Liver/metabolism ; Models, Biological ; Molecular Conformation ; *Phototherapy ; Rats ; Skin/*radiation effects ; Spectrophotometry ; Stereoisomerism
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  • 94
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    Gap junction development is correlated with insulin content in the pancreatic B cell (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-08-29
    Description: The development of gap junctions between insulin-containing B cells was quantitatively analyzed in islets of Langerhans isolated from rats treated with the sulfonylurea glibenclamid for 1, 2, or 7 days. Glibenclamid treatment was associated with a marked depletion of the insulin content of B cells and with an increase in the number and size of gap junctions between these cells. A significance correlation was found between these two events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meda, P -- Halban, P -- Perrelet, A -- Renold, A E -- Orci, L -- New York, N.Y. -- Science. 1980 Aug 29;209(4460):1026-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6773144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication/drug effects ; Female ; Freeze Fracturing ; Glyburide/*pharmacology ; Insulin/*metabolism ; Intercellular Junctions/drug effects/*ultrastructure ; Islets of Langerhans/drug effects/metabolism/*ultrastructure ; Rats
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  • 95
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    Mediation of diurnal fluctuations in pain sensitivity in the rat by food intake patterns: reversal by naloxone (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-10-10
    Description: Rats maintained on a 12-hour light-dark cycle were tested for pain sensitivity after being deprived of food during either the dark or the light phase of the cycle. Diurnal fluctuations in pain sensitivity were observed. The fluctuations followed food intake patterns rather than a natural circadian rhythm, with food deprivation producing a decrease in pain sensitivity. The analgesic response produced by this mild food deprivation was strongly attenuated by naloxone or feeding, suggesting that endogenous opioid systems may be related to patterns of food intake.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGivern, R F -- Berntson, G G -- New York, N.Y. -- Science. 1980 Oct 10;210(4466):210-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7191143" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Circadian Rhythm ; Endorphins/antagonists & inhibitors/*physiology ; Feeding Behavior/*physiology ; Food Deprivation ; Male ; Naloxone/*pharmacology ; Pain/*physiopathology ; Rats
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  • 96
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    Stress-induced eating is mediated through endogenous opiates (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-09-12
    Description: The interaction of endogenous opiates and stress-induced eating in rats was evaluated by pharmacological manipulation. Eating induced by the tail-pinch method was inhibited by the opitate antagonist naloxone; after being repeatedly stressed over a 10-day period and then given nalozone, the rats behaved in a manner indistinguishable from the "wet-dog" shakes of opiate withdrawal. Thus endogenous opiates may have a role in the control of stress-related eating, a finding that may have therapeutic implications for humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morley, J E -- Levine, A S -- New York, N.Y. -- Science. 1980 Sep 12;209(4462):1259-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6250222" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/drug effects ; Cholecystokinin/pharmacology ; Diazepam/pharmacology ; Eating/*drug effects ; Endorphins/antagonists & inhibitors/*physiology ; Male ; Naloxone/*pharmacology ; Rats ; Receptors, Opioid/drug effects ; Stress, Physiological/*physiopathology
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  • 97
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    Intercellular adhesion: coconstruction of contractile heart tissue by cells of different species (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-06-06
    Description: Dissociated embryonic rat myocardial cells and chick myocardial cells labeled with radioactive isotope coaggregate and establish intercellular junctions. These bispecific cells reconstruct synchronously beating myocardial tissue within 24 hours of culture.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nag, A C -- Cheng, M -- New York, N.Y. -- Science. 1980 Jun 6;208(4448):1150-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7375923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion ; *Cell Aggregation ; Cells, Cultured ; Chickens ; Heart/*embryology ; Intercellular Junctions/ultrastructure ; Mosaicism ; Myocardial Contraction ; Myocardium/*cytology ; Rats ; Species Specificity
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  • 98
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    Mild cold exposure increases survival in rats with medial preoptic lesions (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-04-18
    Description: High mortality rate in rats with large medial preoptic lesions discourage their use in studies of brain function. However, virtually all such animals (six out of seven) survived indefinitely if kept at an ambient temperature of 15 degrees C for 2 hours before and 10 to 12 hours after the lesions were made. Although these rats appeared otherwise healthy, they could not maintain normal both temperatures in short-term cold tests. In contrast, five of the nine rats kept at 25 degrees C died within 10 hours after the operation, and three more died within 5 days. Rats kept at 25 degrees C had a much higher incidence of cardiac arrhythmias than did rats kept at 15 degrees C, which may be responsible for their higher moratlity rates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nagel, J A -- Satinoff, E -- New York, N.Y. -- Science. 1980 Apr 18;208(4441):301-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7367860" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Body Temperature Regulation ; Brain/physiology ; *Cold Temperature ; Female ; Heart Rate ; Hypothalamus/*physiology ; Male ; Motor Activity/physiology ; Oxygen Consumption ; Preoptic Area/*physiology/surgery ; Rats ; Vasoconstriction
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  • 99
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    Vitamin D deficiency inhibits pancreatic secretion of insulin (1980)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1980-08-15
    Description: The effects of a vitamin D deficiency on insulin and glucagon release was determined in the isolated perfused rat pancreas by radioimmunoassay of the secreted proteins. During a 30-minute period of perfusion with glucose and arginine, pancreases from vitamin D-deficient rats exhibited a 48 percent reduction in insulin secretion compared to that for pancreases from vitamin D-deficient rats that had been replenished with vitamin D. Vitamin D status had no effect on pancreatic glucagon secretion. This result, along with the previously demonstrated presence in the pancreas of a vitamin D-dependent calcium-binding protein and cytosol receptor for the hormonal form of vitamin D, 1,25-dihydroxyvitamin D3, indicates an important role for vitamin D in the endocrine functioning of the pancreas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norman, A W -- Frankel, J B -- Heldt, A M -- Grodsky, G M -- New York, N.Y. -- Science. 1980 Aug 15;209(4458):823-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6250216" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine/pharmacology ; Cholecalciferol/*deficiency ; Glucagon/secretion ; Glucose/pharmacology ; Insulin/*secretion ; Islets of Langerhans/*secretion ; Rats ; Time Factors ; Vitamin D Deficiency/*metabolism
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  • 100
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    Feeding: satiety signal from intestine triggers brain's noradrenergic mechanism (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-08-29
    Description: Noradrenergic neurons in the hypothalamus involved in feeding and satiety are activated by gastrointestinal receptors. In the unrestrained rat, sites were first identified at which norepinephrine injected in the medial hypothalamus caused spontaneous feeding, or in the lateral hypothalamus caused no response. The activity of in vivo norepinephrine at these two sites was characterized by localized push-pull perfusion. When a nutrient was infused directly into the rat's duodenum, the synaptic release of hypothalamic norepinephrine was enhanced at lateral sites insensitive to norepinephrine, but suppressed at medial sites reactive to norepinephrine. Thus, signals from duodenal receptors are conceivably sent to the rat's brain to end feeding by way of noradrenergic inhibitory neurons in the hypothalamus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, R D -- McCaleb, M L -- New York, N.Y. -- Science. 1980 Aug 29;209(4460):1035-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7403866" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Duodenum/innervation/*physiology ; Feeding Behavior/physiology ; Glucose ; Hypothalamus/*physiology ; Norepinephrine/*physiology ; Rats ; Satiation/*physiology ; Satiety Response/*physiology ; Time Factors
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