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Recent evidence suggests that nectin\u20103, a cell adhesion molecule, mediates memory dysfunction and dendritic alterations in the adult hippocampus induced by postnatal stress. But it is unknown whether postnatal nectin\u20103 reduction alone is sufficient to alter hippocampal structure and function in adulthood. Here, we down regulated hippocampal expression of nectin\u20103 and its heterophilic adhesion partner nectin\u20101, respectively, from early postnatal stage by injecting adeno\u2010associated virus (AAV) into the cerebral lateral ventricles of neonatal mice (postnatal day 2). We found that suppression of nectin\u20103, but not nectin\u20101, expression from the early postnatal stage impaired hippocampus\u2010dependent novel object recognition and spatial object recognition in adult mice. Moreover, AAV\u2010mediated nectin\u20103 knockdown significantly reduced dendritic complexity and spine density of pyramidal neurons throughout the hippocampus, whereas nectin\u20101 knockdown only induced the loss of stubby spines in CA3. Our data provide direct evidence that nectins, especially nectin\u20103, are necessary for postnatal hippocampal development of memory functions and structural integrity.<\/jats:p>","DOI":"10.1002\/hipo.23098","type":"journal-article","created":{"date-parts":[[2019,5,8]],"date-time":"2019-05-08T09:40:49Z","timestamp":1557308449000},"page":"1063-1074","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Postnatal nectin\u20103 knockdown induces structural abnormalities of hippocampal principal neurons and memory deficits in adult mice"],"prefix":"10.1002","volume":"29","author":[{"given":"Rui","family":"Liu","sequence":"first","affiliation":[{"name":"National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital\/Institute of Mental Health) and the Key Laboratory of Mental Health Ministry of Health (Peking University)  Beijing 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