Vasopressin receptor blockade in the anterior hypothalamus suppresses aggression in hamsters

Although the anterior hypothalamus has been implicated in the control of aggression in various rodent species, little is known about the neurochemical mechanisms mediating this control. It has been established that flank marking, which occurs with high frequency during agonistic encounters in hamsters, is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus. The present study was undertaken to determine whether intraspecific aggression in this species is similarly influenced by vasopressin in this area of the hypothalamus. Adult male hamsters, surgically implanted with guide cannulae aimed at the anterior hypothalamus, were microinjected with three different concentrations of the V1-receptor antagonist d(CH2)5Tyr(Me)AVP or a vehicle control of 0.9% NaCl. Sixty minutes after each microinjection a smaller male hamster was introduced into the home cage of the treated hamster. The resident hamsters showed a significant dose-dependent reduction in the number of biting attacks on the intruders over the 10 minute test period. The V1-receptor antagonist also caused a significant increase in the resident hamster's latencies to attack the intruder. However, the resident hamsters' total contact time with the intruder was unaffected by drug treatment suggesting that the reduction of aggression was not due to a generalized effect upon social behavior. The specificity of the drug treatment was further supported by the observation that it did not affect resident hamsters' sexual motivation or ability to mount a receptive female. These data suggest that vasopressin-sensitive neurons in the anterior hypothalamus are involved in the control of intraspecific aggression in male hamsters.