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Wang, X.D.* ; Su, Y.A.* ; Wagner, K.V.* ; Avrabos, C.* ; Scharf, S.H.* ; Hartmann, J.* ; Wolf, M.* ; Liebl, C.* ; Kühne, C.* ; Wurst, W. ; Holsboer, F.* ; Eder, M.* ; Deussing, J.M.* ; Müller, M.B.* ; Schmidt, M.V.*

Nectin-3 links CRHR1 signaling to stress-induced memory deficits and spine loss.

Nat. Neurosci. 16, 706-713 (2013)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter 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
Zeitschrift Nature Neuroscience
Quellenangaben Band: 16, Heft: 6, Seiten: 706-713 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Begutachtungsstatus