| First Author | Wang XD | Year | 2013 |
| Journal | Nat Neurosci | Volume | 16 |
| Issue | 6 | Pages | 706-13 |
| PubMed ID | 23644483 | Mgi Jnum | J:203358 |
| Mgi Id | MGI:5526889 | Doi | 10.1038/nn.3395 |
| Citation | Wang XD, et al. (2013) Nectin-3 links CRHR1 signaling to stress-induced memory deficits and spine loss. Nat Neurosci 16(6):706-13 |
| abstractText | 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. |
