<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11(1)</volume><submitter>Xiao L</submitter><funding>U.S. Department of Health &amp;amp; Human Services | NIH | Eunice Kennedy Shriver National Institute of Child Health and Human Development</funding><pubmed_abstract>Stress leads to brain pathology including hippocampal degeneration, cognitive dysfunction, and potential mood disorders. Hippocampal CA3, a most stress-vulnerable region, consists of pyramidal neurons that regulate cognitive functions e.g. learning and memory. These CA3 neurons express high levels of the neuroprotective protein, neurotrophic factor-α1 (NF-α1), also known as carboxypeptidase E (CPE), and receive contacts from granule cell projections that release BDNF which has neuroprotective activity. Whether NF-α1-CPE and/or BDNF are critical in protecting these CA3 neurons against severe stress-induced cell death is unknown. Here we show that social combined with the physical stress of maternal separation, ear tagging, and tail snipping at weaning in 3-week-old mice lacking NF-α1-CPE, l</pubmed_abstract><journal>Translational psychiatry</journal><pagination>24</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7791060</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Neurotrophic factor-α1, a novel tropin is critical for the prevention of stress-induced hippocampal CA3 cell death and cognitive dysfunction in mice: comparison to BDNF.</pubmed_title><pmcid>PMC7791060</pmcid><pubmed_authors>Sharma VK</pubmed_authors><pubmed_authors>Yang X</pubmed_authors><pubmed_authors>Lee C</pubmed_authors><pubmed_authors>Toulabi L</pubmed_authors><pubmed_authors>Xiao L</pubmed_authors><pubmed_authors>Abebe D</pubmed_authors><pubmed_authors>Arnaoutova I</pubmed_authors><pubmed_authors>Lou H</pubmed_authors><pubmed_authors>Peltekian A</pubmed_authors><pubmed_authors>Loh YP</pubmed_authors></additional><is_claimable>false</is_claimable><name>Neurotrophic factor-α1, a novel tropin is critical for the prevention of stress-induced hippocampal CA3 cell death and cognitive dysfunction in mice: comparison to BDNF.</name><description>Stress leads to brain pathology including hippocampal degeneration, cognitive dysfunction, and potential mood disorders. Hippocampal CA3, a most stress-vulnerable region, consists of pyramidal neurons that regulate cognitive functions e.g. learning and memory. These CA3 neurons express high levels of the neuroprotective protein, neurotrophic factor-α1 (NF-α1), also known as carboxypeptidase E (CPE), and receive contacts from granule cell projections that release BDNF which has neuroprotective activity. Whether NF-α1-CPE and/or BDNF are critical in protecting these CA3 neurons against severe stress-induced cell death is unknown. Here we show that social combined with the physical stress of maternal separation, ear tagging, and tail snipping at weaning in 3-week-old mice lacking NF-α1-CPE, l</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jan</publication><modification>2025-04-25T20:47:46.941Z</modification><creation>2021-02-20T22:09:01Z</creation></dates><accession>S-EPMC7791060</accession><cross_references><pubmed>33414376</pubmed><doi>10.1038/s41398-020-01112-w</doi></cross_references></HashMap>