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  • 1
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    Detyrosinated microtubules buckle and bear load in contracting cardiomyocytes (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    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
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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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
    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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  • 4
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    Nucleus accumbens D2R cells signal prior outcomes and control risky decision-making (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-24
    Description: A marked bias towards risk aversion has been observed in nearly every species tested. A minority of individuals, however, instead seem to prefer risk (repeatedly choosing uncertain large rewards over certain but smaller rewards), and even risk-averse individuals sometimes opt for riskier alternatives. It is not known how neural activity underlies such important shifts in decision-making--either as a stable trait across individuals or at the level of variability within individuals. Here we describe a model of risk-preference in rats, in which stable individual differences, trial-by-trial choices, and responses to pharmacological agents all parallel human behaviour. By combining new genetic targeting strategies with optical recording of neural activity during behaviour in this model, we identify relevant temporally specific signals from a genetically and anatomically defined population of neurons. This activity occurred within dopamine receptor type-2 (D2R)-expressing cells in the nucleus accumbens (NAc), signalled unfavourable outcomes from the recent past at a time appropriate for influencing subsequent decisions, and also predicted subsequent choices made. Having uncovered this naturally occurring neural correlate of risk selection, we then mimicked the temporally specific signal with optogenetic control during decision-making and demonstrated its causal effect in driving risk-preference. Specifically, risk-preferring rats could be instantaneously converted to risk-averse rats with precisely timed phasic stimulation of NAc D2R cells. These findings suggest that individual differences in risk-preference, as well as real-time risky decision-making, can be largely explained by the encoding in D2R-expressing NAc cells of prior unfavourable outcomes during decision-making.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zalocusky, Kelly A -- Ramakrishnan, Charu -- Lerner, Talia N -- Davidson, Thomas J -- Knutson, Brian -- Deisseroth, Karl -- 1F31MH105151-01/MH/NIMH NIH HHS/ -- 1F32MH105053-01/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 31;531(7596):642-6. doi: 10.1038/nature17400. Epub 2016 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bioengineering Department, Stanford University, Stanford, California 94305, USA. ; Neurosciences Program, Stanford University, Stanford, California 94305, USA. ; CNC Program, Stanford University, Stanford, California 94305, USA. ; Psychology Department, Stanford University, Stanford, California 94305, USA. ; Howard Hughes Medical Institute, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27007845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Choice Behavior ; *Decision Making ; Humans ; Individuality ; Male ; Models, Animal ; Models, Neurological ; Models, Psychological ; Neurons/*metabolism ; Nucleus Accumbens/*cytology/*metabolism ; Rats ; Rats, Long-Evans ; Receptors, Dopamine D2/*metabolism ; Reward ; *Risk Management ; Signal Transduction ; Uncertainty
    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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    Unconventional endocannabinoid signaling governs sperm activation via the sex hormone progesterone (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    C9orf72 is required for proper macrophage and microglial function in mice (2016)
    American Association for the Advancement of Science (AAAS)
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    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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  • 7
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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
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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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
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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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
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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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
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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