Vasopressin and serotonin interactions in the control of agonistic behavior.

In hamsters, dominant/subordinate relationships are initially determined by overt aggression, but subsequently communicated by flank marking, an arginine vasopressin (AVP)-dependent behavior. Once a relationship is established, dominant males will flank mark at a higher frequency than their subordinate partners. Flank marking displayed during social encounters can be turned "on or off" by microinjection of AVP or AVP-receptor antagonist within the anterior hypothalamus (AH). For instance, microinjecting dominant hamsters with AVP-receptor antagonist blocks their flank marking and provokes an immediate induction of flank marking by subordinate animals. The central effects of AVP have been extended to include a role in offensive aggression. Microinjection of AVP-receptor antagonist into the AH inhibits the aggression of a resident hamster toward an intruder and diminishes aggression between hamsters placed into a neutral arena. Microinjection of AVP into the ventrolateral hypothalamus (VLH) facilitates offensive aggression of a resident toward an intruder. As AVP receptors in the VLH are testosterone-dependent, it is possible that the reduction of aggression observed in castrated hamsters is due to a loss of AVP responsiveness in the VLH. Recent work has focused on the notion that serotonin (5-HT) antagonizes AVP activity in the CNS. The AH and VLH have a high density of 5-HT terminals and binding sites. Indeed, there appear to be 5-HT synapses on AVP neurons in the AH. Microinjection of 5-HT into the AH inhibits AVP-induced flank marking while IP injection of fluoxetine a serotonin reuptake inhibitor inhibits AVP-induced offensive aggression in the VLH. It is possible that serotonin interacts with AVP to modulate offensive aggression.