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reviously, we have used developmentally immature Syrian hamsters (Mesocricetus auratus) as an animal model to examine the link between repeated adolescent anabolic/androgenic steroid (AAS) exposure and the behavioral neurobiology of offensive aggression [12], [25], [26], [27], [28], [33], [67], [68]. Behavioral data from these studies showed that adolescent hamsters repeatedly exposed to AAS (5.0 mg/kg/day) display significantly high levels of offensive aggression characterized by intense bouts of biting and attacking primarily directed towards the flanks, rump and ventrum of the intruder, as well as high amounts of upright offensive postures and lateral attacks toward the intruder. The finding that adolescent AAS-treated hamsters demonstrated highly escalated and mature forms of offensive aggression in the absence of prior social interactions and established dominance cues suggested that adolescent AAS exposure stimulated aggression directly, perhaps by impacting the development and/or activity of select brain regions that regulate this behavior.

In hamsters, the anterior hypothalamus (AH) appears to be at the center of a neural network of reciprocal connections between the lateral septum (LS), medial amygdala (MeA) and ventrolateral hypothalamus (VLH) that regulates offensive aggression [13]. The activity of the entire network is regulated (at least partially) by the activity of centrally released arginine vasopressin (AVP) and serotonin (5HT) within the AH. In this instance, AH AVP activity has been shown to facilitate offensive aggression that is normally inhibited by AH 5HT [19]. The AH appears also to be an important point of convergence for AAS-induced developmental changes in the AVP and 5HT neural systems that correlate with the emergence of the aggressive phenotype. For example, recently we have shown that aggressive, adolescent AAS-treated hamsters display significant elevations in AVP afferent fiber density and peptide content in the AH commensurate with deficits in 5HT afferent innervation and alterations in 5HT1A and 1B receptor expression in this same brain site as compared to non-aggressive, sesame oil-treated littermates [25], [26], [33], [67]. Further, in mice and hamsters, increased aggressive behavior correlates with higher γ-aminobutyric acid (GABA) activity, levels and density of synaptic terminals containing glutamic acid decarboxylase-65 (i.e., the rate-limiting enzyme in the synthesis of GABA) [28], [34], [64], [70]. Aggressive, adolescent AAS-treated hamsters display significant increases in GAD65-containing afferent terminals in several aggression regions, including the anterior hypothalamus [28]. It is possible that, either together or alone, these adolescent AAS-induced neurodevelopmental changes stimulate offensive aggression by permanently altering the activation patterns of neurons in these discrete forebrain regions. To date, however, it is unknown whether adolescent AAS exposure activates neurons in these brain areas important for aggression control.

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