title: The social deficits of the oxytocin knockout mouse.
abstract: Numerous studies have implicated oxytocin (OT) and oxytocin receptors in the central mediation of social cognition and social behavior. Much of our understanding of OT's central effects depends on pharmacological studies with OT agonists and antagonists. Recently, our knowledge of OT's effects has been extended by the development of oxytocin knockout (OTKO) mice. Mice with a null mutation of the OT gene manifest several interesting cognitive and behavioral changes, only some of which were predicted by pharmacological studies. Contrary to studies in rats, mice do not appear to require OT for normal sexual or maternal behavior, though OT is necessary for the milk ejection reflex during lactation. OTKO pups thrive if raised by a lactating female, but OTKO pups emit fewer ultrasonic vocalizations with maternal separation and OTKO adults are more aggressive than WT mice. Remarkably, OTKO mice fail to recognize familiar conspecifics after repeated social encounters, though olfactory and non-social memory functions appear to be intact. Central OT administration into the amygdala restores social recognition. The development of transgenic mice with specific deficits in social memory represents a promising approach to examine the cellular and neural systems of social cognition. These studies may provide valuable new perspectives on diseases characterized by social deficits, such as autism or reactive attachment disorder.
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D001923:Brain Chemistry / Q000235:genetics; D005260:Female; D008297:Male; D008425:Maternal Behavior / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D010121:Oxytocin / Q000235:genetics* / Q000378:metabolism / Q000502:physiology*; D010641:Phenotype; D051381:Rats; D012919:Social Behavior; D014018:Tissue Distribution
chemical_list: D010121:Oxytocin