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Open Access Green as soon as Postprint is submitted to ZB.
Nectin-3 links CRHR1 signaling to stress-induced memory deficits and spine loss.
Nat. Neurosci. 16, 706-713 (2013)
Stress impairs cognition via corticotropin-releasing hormone receptor 1 (CRHR1), but the molecular link between abnormal CRHR1 signaling and stress-induced cognitive impairments remains unclear. We investigated whether the cell adhesion molecule nectin-3 is required for the effects of CRHR1 on cognition and structural remodeling after early-life stress exposure. Postnatally stressed adult mice had decreased hippocampal nectin-3 levels, which could be attenuated by CRHR1 inactivation and mimicked by corticotropin-releasing hormone (CRH) overexpression in forebrain neurons. Acute stress dynamically reduced hippocampal nectin-3 levels, which involved CRH-CRHR1, but not glucocorticoid receptor, signaling. Suppression of hippocampal nectin-3 caused spatial memory deficits and dendritic spine loss, whereas enhancing hippocampal nectin-3 expression rescued the detrimental effects of early-life stress on memory and spine density in adulthood. Our findings suggest that hippocampal nectin-3 is necessary for the effects of stress on memory and structural plasticity and indicate that the CRH-CRHR1 system interacts with the nectin-afadin complex to mediate such effects.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Corticotropin-releasing Hormone ; Early-life Stress ; Anxiety-related Behavior ; Cell-adhesion Molecules ; Cognitive Deficits ; Dendritic Spines ; Receptor 1 ; Hippocampus ; Maintenance ; Mechanisms
ISSN (print) / ISBN
1097-6256
e-ISSN
1546-1726
Journal
Nature Neuroscience
Quellenangaben
Volume: 16,
Issue: 6,
Pages: 706-713
Publisher
Nature Publishing Group
Non-patent literature
Publications
Reviewing status
Peer reviewed