ROLE OF THE CENTRAL AMYGDALA IN SOCIAL COMMUNICATION IN SYRIAN-HAMSTERS (MESOCRICETUS-AURATUS)

In Syrian hamsters, vasopressin (AVP) controls a form of scent marking called flank marking. Microinjection and lesion studies have identifi ed several components of the neural circuit controlling this behavior. Microinjection of AVP into the medial preoptic-anterior hypothalamus (MPOA-AH), lateral septal nucleus (LS), bed nucleus of stria terminali s (BNST), and periaqueductal gray (PAG) stimulates an intense bout of flank marking. Lesions of areas such as the MPOA-AH and the LS inhibit flank marking. Other studies employing Fos immunocytochemistry sugges t that the central amygdala (Ce) might be a component of this neural c ircuit. The purpose of the present study was to assess the significanc e of the Ce in regulation of AVP-induced flank marking. In Expt. 1A, t he Ce of hamsters were either lesioned with ibotenic acid or sham-lesi oned. In Expt. 1B, the Ce of hamsters were either lesioned electrolyti cally or sham-lesioned. All lesions were made bilaterally. One week la ter, hamsters were microinjected with AVP into the MPOA-AH and immedia tely tested for flank marking. In Expt. 2, the hamsters were microinje cted with AVP into the Ce and were immediately tested for flank markin g. Ibotenic lesions of the Ce reduced flank marking and electrolytic l esions completely inhibited flank marking in response to AVP microinje cted into the MPOA-AH. Sham-lesions or lesions placed in other areas o f the amygdala resulted in intense bouts of AVP-induced flank marking and flank grooming. No flank marking or flank grooming was observed in response to AVP microinjected into the Ce. These data indicate that t he Ce plays a critical role in AVP-induced flank marking, although fla nk marking is not induced by AVP within the Ce itself.