title: Pervasive social deficits, but normal parturition, in oxytocin receptor-deficient mice.
abstract: The oxytocin receptor (OXTR) and its ligand, oxytocin (OXT), regulate reproductive physiology (i.e., parturition and lactation) and sociosexual behaviors. To define the essential functions of OXTR, we generated mice with a null mutation in the Oxtr gene (Oxtr(-/-)) and compared them with OXT-deficient (Oxt(-/-)) mice. Oxtr(-/-) mice were viable and had no obvious deficits in fertility or reproductive behavior. Oxtr(-/-) dams exhibited normal parturition but demonstrated defects in lactation and maternal nurturing. Infant Oxtr(-/-) males emitted fewer ultrasonic vocalizations than wild-type littermates in response to social isolation. Adult Oxtr(-/-) males also showed deficits in social discrimination and elevated aggressive behavior. Ligand Oxt(-/-) males from Oxt(-/-) dams, but not from Oxt(+/-) dams, showed similar high levels of aggression. These data suggest a developmental role for the OXT/OXTR system in shaping adult aggressive behavior. Our studies demonstrate that OXTR plays a critical role in regulating several aspects of social behavior and may have important implications for developmental psychiatric disorders characterized by deficits in social behavior.
authors.affiliation: Laboratory of Molecular Biology, Department of Molecular and Cell Biology, Graduate School of Agricultural Science, Tohoku University, 1-1 Tsutsumidori-Amamiyamachi, Aoba-ku, Sendai, Miyagi 981-8555, Japan.
authors.forename: Yuki
authors.initials: Y
authors.lastname: Takayanagi
authors.forename: Masahide
authors.initials: M
authors.lastname: Yoshida
authors.forename: Isadora F
authors.initials: IF
authors.lastname: Bielsky
authors.forename: Heather E
authors.initials: HE
authors.lastname: Ross
authors.forename: Masaki
authors.initials: M
authors.lastname: Kawamata
authors.forename: Tatsushi
authors.initials: T
authors.lastname: Onaka
authors.forename: Teruyuki
authors.initials: T
authors.lastname: Yanagisawa
authors.forename: Tadashi
authors.initials: T
authors.lastname: Kimura
authors.forename: Martin M
authors.initials: MM
authors.lastname: Matzuk
authors.forename: Larry J
authors.initials: LJ
authors.lastname: Young
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Nishimori
mesh_terms: D000374:Aggression; D000818:Animals; D005260:Female; D007774:Lactation / Q000235:genetics; D008297:Male; D008425:Maternal Behavior; D051379:Mice; D009154:Mutation; D010121:Oxytocin / Q000172:deficiency / Q000502:physiology; D036801:Parturition; D011247:Pregnancy; D018045:Receptors, Oxytocin / Q000172:deficiency* / Q000235:genetics / Q000502:physiology*; D012920:Social Behavior Disorders / Q000209:etiology* / Q000235:genetics
chemical_list: D018045:Receptors, Oxytocin; D010121:Oxytocin