Intraspecific aggression in male hamsters is inhibited by intrahypothalamic vasopressin‐receptor antagonist

Abstract

The present study examines the effect of the arginine vasopressin (AVP) receptor antagonist, d(CH&Tyr(Me)AVP, on intraspecific aggression between pairs of male Golden hamsters in a neutral territory. Subjects drawn from a group of 24 animals were paired once each with novel partners from the group under each of three experimental conditions: 1) both members of a pair were microinjected into the anterior hypothalamus with saline (SIS), 2) one member of a pair was microinjected with AVP-receptor antagonist and its partner with saline (AIS), and 3) both members of a pair were microinjected with AVP-receptor antagonist (AIA). There were significantly (P < .01) fewer attacks during encounters between pairs of hamsters in the A/A condition compared to pairs in the A/S condition. Similarly, pairs in the A/S condition attacked significantly (P < .025) less often than pairs of hamsters in the SIS condition. These results confivm our earlier work showing that AVP-receptor antagonist reduces intraspecific aggression. In addition, saline-treated hamsters initiated significantly (P < .001) fewer attacks toward antagonist treated hamsters than would have been predicted if their opponent was not drug treated. These latter results suggest that hamsters microinjected into the anterior hypothalamus with an AW-receptor antagonist also elicit less aggression from conspecifics.

Neuroscience of Aggression

“…Interestingly, pair-bonded male prairie voles naturally display aggression toward conspecific females but not toward their female partner and, therefore, selective aggression allows investigation of the neurobiology of femaledirected aggression. Together with previous research from other animals (Ferris et al 1989(Ferris et al , 1997Harrison et al 2000b;Jackson et al 2005;Veenema et al 2006;Grimes et al 2007), these data demonstrate a unique point of convergence in the mammalian brain (Choi et al 2005;Motta et al 2009). 6 Drug abuse impairs formation and maintenance of monogamous pair-bonds.…”

Vasopressin cell groups exhibit strongly divergent responses to copulation and male–male interactions in mice

“…Following aggressive interactions, dominant hamsters exhibit increased AVP-Fos colocalization within the medial SON and NC, both of which project AVP-ir axons into the AH (Delville et al, 2000). As predicted by those findings, offensive aggression in hamsters is blocked by infusions of a V 1a antagonist into either the AH or ventrolateral hypothalamus, whereas aggression is facilitated by infusions of AVP (Ferris and Potegal, 1988; Potegal and Ferris, 1989; Delville et al, 1996; Ferris et al, 1997; Jackson et al, 2005). Similar pharmacological and activation results are obtained for the AH in tests of selective post-mating aggression in male prairie voles (Gobrogge et al, 2007, 2009), and voles exhibit endogenous AVP release within the AH that is positively correlated with aggression (Gobrogge et al, 2009).…”

Plasticity in anterior hypothalamic vasopressin correlates with aggression during anabolic-androgenic steroid withdrawal in hamsters.

“…Adolescent AAS exposure may facilitate and maintain heightened levels of offensive aggression by producing sustained increases in the activity of neurochemical signals involved in this activation of this response. Previous work from our laboratory and the laboratories of others indicate that AH-AVP is a potent activator of offensive aggression in Syrian hamsters (Caldwell & Albers, 2004;Delville et al, 2000;Ferris, 1992;Ferris et al, 1989Ferris et al, , 1997Ferris & Potegal, 1988;Jackson et al, 2005;Potegal & Ferris, 1989). Aggressive, adolescent AAS-treated animals have an altered AH-AVP neural system; specifically, AH-AVP neurons contain more AVP in aggressive, adolescent AAS-treated animals and display increased AVP afferent development to the AH brain region implicated in the control of aggression, suggesting that increased AH-AVP tone underlies the development of the adolescent AAS-induced aggressive phenotype (Harrison et al, 2000).…”