Profound impairment in social recognition and reduction in anxiety-like behavior in vasopressin V1a receptor knockout mice

Considerable evidence suggests that arginine vasopressin (AVP) is critically involved in the regulation of many social and nonsocial behaviors, including emotionality. The existence of two AVP receptors in the brain, namely the VIa and VIb subtypes, and the lack of clear pharmacological data using selective agonists or antagonists, make it difficult to determine which receptor is responsible for the AVP-mediated effects on behavior. Here we report the behavioral effects of a null mutation in the VIa receptor (VIoR) in male mice. Male mice lacking functional VIaR (V I aRKO) exhibit markedly reduced anxiety-like behavior and a profound impairment in social recognition. V IaRKC) performed normally on spatial and nonsocial olfactory learning and memory tasks. Acute central administration of AVP robustly stimulated stereotypical scratching and autogrooming in wild-type (VVT), but not V I aRKO males. AVP and oxytocin (OT) mRNA and OT receptor-binding levels were similar in VVT and V I aRKO mice. Given the current findings, the V I aR may provide a novel potential pharmacological target for social and affective disorders including autism, and anxiety disorders.