Abstract
Chronic anabolic–androgenic steroid (AAS) treatment during adolescence facilitates offensive aggression in male Syrian hamsters ( Mesocricetus auratus). The current study assessed whether adolescent AAS exposure influenced the immunohistochemical localization of glutamic acid decarboxylase (GAD 65), the rate-limiting enzyme in the synthesis of γ-aminobutyric acid (GABA), in areas of hamster brain implicated in aggressive behavior. Hamsters were administered high dose AAS throughout adolescence, scored for offensive aggression, and then examined for differences in GAD 65 puncta to regions of the hamster brain important for aggression. When compared with control animals, aggressive AAS-treated hamsters showed significant increases in the area covered by GAD 65 immunoreactive puncta in several of these aggression regions, including the anterior hypothalamus, ventrolateral hypothalamus, and medial amygdala. Conversely, aggressive AAS-treated hamsters showed a significant decrease in GAD 65-ir puncta in the lateral septum when compared with oil-treated controls. However, no differences in GAD 65 puncta were found in other aggression areas, such as the bed nucleus of the stria terminalis and central amygdala. Together, these results support a role for altered GAD 65 synthesis and function in adolescent AAS-facilitated offensive aggression.
Published Version
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