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  • 1
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    Early neocortical regionalization in the absence of thalamic innervation (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-07
    Description: There is a long-standing controversy regarding the mechanisms that generate the functional subdivisions of the cerebral neocortex. One model proposes that thalamic axonal input specifies these subdivisions; the competing model postulates that patterning mechanisms intrinsic to the dorsal telencephalon generate neocortical regions. Gbx-2 mutant mice, whose thalamic differentiation is disrupted, were investigated. Despite the lack of cortical innervation by thalamic axons, neocortical region-specific gene expression (Cadherin-6, EphA-7, Id-2, and RZR-beta) developed normally. This provides evidence that patterning mechanisms intrinsic to the neocortex specify the basic organization of its functional subdivisions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyashita-Lin, E M -- Hevner, R -- Wassarman, K M -- Martinez, S -- Rubenstein, J L -- NS34661-01A1/NS/NINDS NIH HHS/ -- R01 MH49428-01/MH/NIMH NIH HHS/ -- R01 MH51561-01A1/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):906-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nina Ireland Laboratory of Developmental Neurobiology, Department of Psychiatry, School of Medicine, University of California San Francisco, San Francisco, CA 94143-0984, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10436162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/chemistry/*physiology ; Cadherins/genetics ; Calbindin 2 ; Carbocyanines ; DNA-Binding Proteins/genetics ; Gene Expression ; Homeodomain Proteins/genetics/physiology ; Immunohistochemistry ; In Situ Hybridization ; Inhibitor of Differentiation Proteins ; Lymphoid Enhancer-Binding Factor 1 ; Mice ; Mutation ; Neocortex/anatomy & histology/*embryology/growth & development/metabolism ; Nerve Fibers/physiology/ultrastructure ; Proteins/genetics ; Receptors, Cell Surface/genetics ; Receptors, Cytoplasmic and Nuclear/genetics ; Receptors, Melatonin ; S100 Calcium Binding Protein G/analysis ; Steroid 17-alpha-Hydroxylase/analysis ; Telencephalon/embryology/growth & development/physiology ; Thalamus/anatomy & histology/*embryology/growth & development/metabolism ; Transcription Factors/genetics
    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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  • 2
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    Sorting of striatal and cortical interneurons regulated by semaphorin-neuropilin interactions (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-08-04
    Description: Most striatal and cortical interneurons arise from the basal telencephalon, later segregating to their respective targets. Here, we show that migrating cortical interneurons avoid entering the striatum because of a chemorepulsive signal composed at least in part of semaphorin 3A and semaphorin 3F. Migrating interneurons expressing neuropilins, receptors for semaphorins, are directed to the cortex; those lacking them go to the striatum. Loss of neuropilin function increases the number of interneurons that migrate into the striatum. These observations reveal a mechanism by which neuropilins mediate sorting of distinct neuronal populations into different brain structures, and provide evidence that, in addition to guiding axons, these receptors also control neuronal migration in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marin, O -- Yaron, A -- Bagri, A -- Tessier-Lavigne, M -- Rubenstein, J L -- K02MH01046-01/MH/NIMH NIH HHS/ -- R01DA12462/DA/NIDA NIH HHS/ -- R01MH49428-01/MH/NIMH NIH HHS/ -- R01MH51561-01A1/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2001 Aug 3;293(5531):872-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Nina Ireland Laboratory of Developmental Neurobiology, Langley Porter Psychiatric Institute, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11486090" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basal Ganglia/*cytology/embryology/metabolism ; COS Cells ; Cell Movement ; Cerebral Cortex/*cytology/embryology/metabolism ; Corpus Striatum/*cytology/embryology/metabolism ; Culture Techniques ; Glycoproteins/*metabolism ; Green Fluorescent Proteins ; Interneurons/metabolism/*physiology ; Ligands ; Luminescent Proteins/metabolism ; Membrane Proteins/*metabolism ; Mice ; Mice, Transgenic ; Mutation ; Nerve Tissue Proteins/genetics/*metabolism ; Neuropilin-1 ; Recombinant Proteins/metabolism ; Semaphorin-3A ; Signal Transduction
    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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  • 3
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    Specification of jaw subdivisions by Dlx genes (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-08-24
    Description: The success of vertebrates was due in part to the acquisition and modification of jaws. Jaws are principally derived from the branchial arches, embryonic structures that exhibit proximodistal polarity. To investigate the mechanisms that specify the identity of skeletal elements within the arches, we examined mice lacking expression of Dlx5 and Dlx6, linked homeobox genes expressed distally but not proximally within the arches. Dlx5/6-/- mutants exhibit a homeotic transformation of lower jaws to upper jaws. We suggest that nested Dlx expression in the arches patterns their proximodistal axes. Evolutionary acquisition and subsequent refinement of jaws may have been dependent on modification of Dlx expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Depew, Michael J -- Lufkin, Thomas -- Rubenstein, John L R -- K02MH01046-01/MH/NIMH NIH HHS/ -- T32DE07204/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 2002 Oct 11;298(5592):381-5. Epub 2002 Aug 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nina Ireland Laboratory of Developmental Neurobiology, 401 Parnassus Avenue, University of California, San Francisco, San Francisco, CA 94143-0984, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12193642" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; *Body Patterning ; Branchial Region/embryology/physiology ; Ear Ossicles/embryology ; Gene Deletion ; Gene Expression Regulation, Developmental ; *Genes, Homeobox ; Homeodomain Proteins/*genetics/physiology ; Mandible/anatomy & histology/*embryology ; Maxilla/anatomy & histology/*embryology ; Mice ; Morphogenesis ; Palate/embryology ; Skull/abnormalities/embryology ; Sphenoid Bone/embryology
    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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  • 4
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    Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-11-12
    Description: Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality. Rett syndrome is characterized by apparently normal early development followed by regression, motor abnormalities, seizures and features of autism, especially stereotyped behaviours. The mechanisms mediating these features are poorly understood. Here we show that mice lacking Mecp2 from GABA (gamma-aminobutyric acid)-releasing neurons recapitulate numerous Rett syndrome and autistic features, including repetitive behaviours. Loss of MeCP2 from a subset of forebrain GABAergic neurons also recapitulates many features of Rett syndrome. MeCP2-deficient GABAergic neurons show reduced inhibitory quantal size, consistent with a presynaptic reduction in glutamic acid decarboxylase 1 (Gad1) and glutamic acid decarboxylase 2 (Gad2) levels, and GABA immunoreactivity. These data demonstrate that MeCP2 is critical for normal function of GABA-releasing neurons and that subtle dysfunction of GABAergic neurons contributes to numerous neuropsychiatric phenotypes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057962/" 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/PMC3057962/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chao, Hsiao-Tuan -- Chen, Hongmei -- Samaco, Rodney C -- Xue, Mingshan -- Chahrour, Maria -- Yoo, Jong -- Neul, Jeffrey L -- Gong, Shiaoching -- Lu, Hui-Chen -- Heintz, Nathaniel -- Ekker, Marc -- Rubenstein, John L R -- Noebels, Jeffrey L -- Rosenmund, Christian -- Zoghbi, Huda Y -- 29709/PHS HHS/ -- F31MH078678/MH/NIMH NIH HHS/ -- HD024064/HD/NICHD NIH HHS/ -- HD053862/HD/NICHD NIH HHS/ -- K08 NS052240/NS/NINDS NIH HHS/ -- K08 NS052240-01/NS/NINDS NIH HHS/ -- K08 NS052240-02/NS/NINDS NIH HHS/ -- K08 NS052240-03/NS/NINDS NIH HHS/ -- K08 NS052240-04/NS/NINDS NIH HHS/ -- K08 NS052240-05/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064-22/HD/NICHD NIH HHS/ -- R01 HD062553/HD/NICHD NIH HHS/ -- R01 NS048884/NS/NINDS NIH HHS/ -- R01 NS057819/NS/NINDS NIH HHS/ -- R01 NS057819-04/NS/NINDS NIH HHS/ -- R01 NS057819-05/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 11;468(7321):263-9. doi: 10.1038/nature09582.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉]Department of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068835" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/complications/genetics/pathology/*physiopathology ; Brain/cytology ; Compulsive Behavior/complications/genetics/physiopathology ; Disease Models, Animal ; Electroencephalography ; Genotype ; Glutamate Decarboxylase/metabolism ; Hippocampus/pathology/physiopathology ; Homeodomain Proteins/genetics ; Inhibitory Postsynaptic Potentials ; Long-Term Potentiation ; Male ; Methyl-CpG-Binding Protein 2/*deficiency/genetics/*metabolism ; Mice ; Mice, Transgenic ; Neural Inhibition ; Neuronal Plasticity ; Neurons/metabolism ; Phenotype ; Presynaptic Terminals/metabolism ; Psychomotor Disorders/complications/genetics/physiopathology ; Reflex, Startle/genetics ; Respiration ; Rett Syndrome/complications/genetics/pathology/*physiopathology ; Self-Injurious Behavior/complications/genetics/physiopathology ; *Signal Transduction ; Stereotypic Movement Disorder/complications/genetics/pathology/*physiopathology ; Survival Rate ; Synaptic Transmission ; Vesicular Inhibitory Amino Acid Transport Proteins/genetics ; gamma-Aminobutyric Acid/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    New neurons follow the flow of cerebrospinal fluid in the adult brain (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-18
    Description: In the adult brain, neuroblasts born in the subventricular zone migrate from the walls of the lateral ventricles to the olfactory bulb. How do these cells orient over such a long distance and through complex territories? Here we show that neuroblast migration parallels cerebrospinal fluid (CSF) flow. Beating of ependymal cilia is required for normal CSF flow, concentration gradient formation of CSF guidance molecules, and directional migration of neuroblasts. Results suggest that polarized epithelial cells contribute important vectorial information for guidance of young, migrating neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sawamoto, Kazunobu -- Wichterle, Hynek -- Gonzalez-Perez, Oscar -- Cholfin, Jeremy A -- Yamada, Masayuki -- Spassky, Nathalie -- Murcia, Noel S -- Garcia-Verdugo, Jose Manuel -- Marin, Oscar -- Rubenstein, John L R -- Tessier-Lavigne, Marc -- Okano, Hideyuki -- Alvarez-Buylla, Arturo -- HD 32116/HD/NICHD NIH HHS/ -- NS 28478/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 3;311(5761):629-32. Epub 2006 Jan 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery and Developmental and Stem Cell Biology Program, University of California San Francisco, San Francisco, CA 94143, USA. sawamoto@sc.itc.keio.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16410488" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Tissue Transplantation ; Cell Movement ; Cell Polarity ; Cerebral Ventricles/cytology/physiology ; Cerebrospinal Fluid/*physiology ; Choroid Plexus/secretion ; Cilia/physiology ; Ependyma/cytology/*physiology ; Epithelial Cells/physiology ; Intercellular Signaling Peptides and Proteins ; Mice ; Nerve Tissue Proteins/cerebrospinal fluid ; Neurons/cytology/*physiology ; Olfactory Bulb/cytology/physiology ; Recombinant Fusion Proteins/cerebrospinal fluid
    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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  • 6
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    Interneurons from embryonic development to cell-based therapy (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-04-12
    Description: Many neurologic and psychiatric disorders are marked by imbalances between neural excitation and inhibition. In the cerebral cortex, inhibition is mediated largely by GABAergic (gamma-aminobutyric acid-secreting) interneurons, a cell type that originates in the embryonic ventral telencephalon and populates the cortex through long-distance tangential migration. Remarkably, when transplanted from embryos or in vitro culture preparations, immature interneurons disperse and integrate into host brain circuits, both in the cerebral cortex and in other regions of the central nervous system. These features make interneuron transplantation a powerful tool for the study of neurodevelopmental processes such as cell specification, cell death, and cortical plasticity. Moreover, interneuron transplantation provides a novel strategy for modifying neural circuits in rodent models of epilepsy, Parkinson's disease, mood disorders, and chronic pain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4056344/" 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/PMC4056344/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Southwell, Derek G -- Nicholas, Cory R -- Basbaum, Allan I -- Stryker, Michael P -- Kriegstein, Arnold R -- Rubenstein, John L -- Alvarez-Buylla, Arturo -- HD032116/HD/NICHD NIH HHS/ -- MH049428/MH/NIMH NIH HHS/ -- NS14627/NS/NINDS NIH HHS/ -- NS28478/NS/NINDS NIH HHS/ -- NS78326/NS/NINDS NIH HHS/ -- R01 EY002874/EY/NEI NIH HHS/ -- R01 MH049428/MH/NIMH NIH HHS/ -- R01 NS014627/NS/NINDS NIH HHS/ -- R01 NS028478/NS/NINDS NIH HHS/ -- R01 NS078326/NS/NINDS NIH HHS/ -- R01-EY02874/EY/NEI NIH HHS/ -- R37 HD032116/HD/NICHD NIH HHS/ -- T32 GM008568/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Apr 11;344(6180):1240622. doi: 10.1126/science.1240622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Surgery, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24723614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Separation ; *Cell- and Tissue-Based Therapy ; Cerebral Cortex/cytology/growth & development/physiology ; *Embryonic Development ; Humans ; Interneurons/*physiology/*transplantation ; Mental Disorders/*therapy ; Mice ; Nervous System Diseases/*therapy
    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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  • 7
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    Interneuron migration from basal forebrain to neocortex: dependence on Dlx genes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: Although previous analyses indicate that neocortical neurons originate from the cortical proliferative zone, evidence suggests that a subpopulation of neocortical interneurons originates within the subcortical telencephalon. For example, gamma-aminobutyric acid (GABA)-expressing cells migrate in vitro from the subcortical telencephalon into the neocortex. The number of GABA-expressing cells in neocortical slices is reduced by separating the neocortex from the subcortical telencephalon. Finally, mice lacking the homeodomain proteins DLX-1 and DLX-2 show no detectable cell migration from the subcortical telencephalon to the neocortex and also have few GABA-expressing cells in the neocortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, S A -- Eisenstat, D D -- Shi, L -- Rubenstein, J L -- K02 MH01046/MH/NIMH NIH HHS/ -- R01 MH51561/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):474-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nina Ireland Laboratory of Developmental Neurobiology, Center for Neurobiology and Psychiatry, Department of Psychiatry, University of California at San Francisco, CA 94143-0984, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334308" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calbindins ; Cell Movement ; Corpus Striatum/*cytology/embryology/metabolism ; Culture Techniques ; DNA-Binding Proteins/*genetics/physiology ; *Genes, Homeobox ; Glutamate Decarboxylase/metabolism ; Homeodomain Proteins/*genetics/physiology ; Interneurons/chemistry/*physiology ; Mice ; Mutation ; Neocortex/*cytology/embryology/metabolism ; S100 Calcium Binding Protein G/analysis ; Telencephalon/*cytology/embryology/metabolism ; Transcription Factors ; gamma-Aminobutyric Acid/analysis
    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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  • 8
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    Patterning and plasticity of the cerebral cortex (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-08
    Description: The cerebral cortex of the human brain is a sheet of about 10 billion neurons divided into discrete subdivisions or areas that process particular aspects of sensation, movement, and cognition. Recent evidence has begun to transform our understanding of how cortical areas form, make specific connections with other brain regions, develop unique processing networks, and adapt to changes in inputs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sur, Mriganka -- Rubenstein, John L R -- New York, N.Y. -- Science. 2005 Nov 4;310(5749):805-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, 77 Massachusetts Ave., 46-6237, Cambridge, MA 02139, USA. msur@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16272112" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; *Body Patterning ; Brain Mapping ; Cerebral Cortex/anatomy & histology/*growth & development/metabolism/*physiology ; Dominance, Ocular ; Gene Expression Regulation, Developmental ; Humans ; Models, Neurological ; Morphogenesis ; Nerve Net/physiology ; Neural Pathways/growth & development/physiology ; *Neuronal Plasticity ; Thalamus/anatomy & histology/growth & development/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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  • 9
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    Autistic-like behaviour in Scn1a+/- mice and rescue by enhanced GABA-mediated neurotransmission (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-08-24
    Description: Haploinsufficiency of the SCN1A gene encoding voltage-gated sodium channel Na(V)1.1 causes Dravet's syndrome, a childhood neuropsychiatric disorder including recurrent intractable seizures, cognitive deficit and autism-spectrum behaviours. The neural mechanisms responsible for cognitive deficit and autism-spectrum behaviours in Dravet's syndrome are poorly understood. Here we report that mice with Scn1a haploinsufficiency exhibit hyperactivity, stereotyped behaviours, social interaction deficits and impaired context-dependent spatial memory. Olfactory sensitivity is retained, but novel food odours and social odours are aversive to Scn1a(+/-) mice. GABAergic neurotransmission is specifically impaired by this mutation, and selective deletion of Na(V)1.1 channels in forebrain interneurons is sufficient to cause these behavioural and cognitive impairments. Remarkably, treatment with low-dose clonazepam, a positive allosteric modulator of GABA(A) receptors, completely rescued the abnormal social behaviours and deficits in fear memory in the mouse model of Dravet's syndrome, demonstrating that they are caused by impaired GABAergic neurotransmission and not by neuronal damage from recurrent seizures. These results demonstrate a critical role for Na(V)1.1 channels in neuropsychiatric functions and provide a potential therapeutic strategy for cognitive deficit and autism-spectrum behaviours in Dravet's syndrome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3448848/" 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/PMC3448848/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, Sung -- Tai, Chao -- Westenbroek, Ruth E -- Yu, Frank H -- Cheah, Christine S -- Potter, Gregory B -- Rubenstein, John L -- Scheuer, Todd -- de la Iglesia, Horacio O -- Catterall, William A -- R01 MH075016/MH/NIMH NIH HHS/ -- R01 NS025704/NS/NINDS NIH HHS/ -- R01 NS25704/NS/NINDS NIH HHS/ -- R37 MH049428/MH/NIMH NIH HHS/ -- England -- Nature. 2012 Sep 20;489(7416):385-90. doi: 10.1038/nature11356. Epub 2012 Aug 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Neurobiology & Behavior, University of Washington, Seattle, Washington 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22914087" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/physiopathology ; Autistic Disorder/complications/*drug therapy/genetics/*physiopathology ; Clonazepam/pharmacology/therapeutic use ; Epilepsies, Myoclonic/complications/genetics/physiopathology ; GABA Modulators/pharmacology/*therapeutic use ; GABAergic Neurons/metabolism ; Haploinsufficiency/genetics ; Heterozygote ; Hippocampus/cytology ; Homeodomain Proteins/genetics ; Hyperkinesis/physiopathology ; Interneurons/metabolism ; Male ; Memory ; Mice ; NAV1.1 Voltage-Gated Sodium Channel ; Nerve Tissue Proteins/*genetics/*metabolism ; Social Behavior ; Sodium Channels/*genetics/*metabolism ; Space Perception ; Stereotypic Movement Disorder/physiopathology ; Synaptic Transmission/*drug effects ; Syndrome ; Transcription Factors/genetics ; gamma-Aminobutyric Acid/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    Intrinsically determined cell death of developing cortical interneurons (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-10-09
    Description: Cortical inhibitory circuits are formed by gamma-aminobutyric acid (GABA)-secreting interneurons, a cell population that originates far from the cerebral cortex in the embryonic ventral forebrain. Given their distant developmental origins, it is intriguing how the number of cortical interneurons is ultimately determined. One possibility, suggested by the neurotrophic hypothesis, is that cortical interneurons are overproduced, and then after their migration into cortex the excess interneurons are eliminated through a competition for extrinsically derived trophic signals. Here we characterize the developmental cell death of mouse cortical interneurons in vivo, in vitro and after transplantation. We found that 40% of developing cortical interneurons were eliminated through Bax (Bcl-2-associated X)-dependent apoptosis during postnatal life. When cultured in vitro or transplanted into the cortex, interneuron precursors died at a cellular age similar to that at which endogenous interneurons died during normal development. Over transplant sizes that varied 200-fold, a constant fraction of the transplanted population underwent cell death. The death of transplanted neurons was not affected by the cell-autonomous disruption of TrkB (tropomyosin kinase receptor B), the main neurotrophin receptor expressed by neurons of the central nervous system. Transplantation expanded the cortical interneuron population by up to 35%, but the frequency of inhibitory synaptic events did not scale with the number of transplanted interneurons. Taken together, our findings indicate that interneuron cell death is determined intrinsically, either cell-autonomously or through a population-autonomous competition for survival signals derived from other interneurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3726009/" 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/PMC3726009/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Southwell, Derek G -- Paredes, Mercedes F -- Galvao, Rui P -- Jones, Daniel L -- Froemke, Robert C -- Sebe, Joy Y -- Alfaro-Cervello, Clara -- Tang, Yunshuo -- Garcia-Verdugo, Jose M -- Rubenstein, John L -- Baraban, Scott C -- Alvarez-Buylla, Arturo -- F32NS061497/NS/NINDS NIH HHS/ -- R01 NS048528/NS/NINDS NIH HHS/ -- R01 NS071785/NS/NINDS NIH HHS/ -- T32 GM007618/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Nov 1;491(7422):109-13. doi: 10.1038/nature11523. Epub 2012 Oct 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Graduate Program, University of California, San Francisco, California 94143, USA. dereksouthwell@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23041929" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; *Apoptosis ; Caspase 3/metabolism ; Cell Aging/physiology ; Cell Count ; Cell Survival ; Female ; Inhibitory Postsynaptic Potentials ; Interneurons/*cytology/metabolism/transplantation ; Male ; Membrane Glycoproteins/deficiency/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Neocortex/*cytology/growth & development ; Neural Stem Cells/cytology/metabolism/transplantation ; Protein-Tyrosine Kinases/deficiency/genetics/metabolism ; Pyramidal Cells/cytology/metabolism ; bcl-2-Associated X Protein/deficiency/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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