Mercaptoacetate-induced feeding is impaired by central nucleus of the amygdala lesions.

Systemic administration of mercaptoacetate (MA) blocks beta oxidation of fatty acids and stimulates food intake. The present experiment examined MA-induced feeding in rats with bilateral lesions of the central nucleus of the amygdala (CNA) and sham-operated controls. Food intake was measured for 6 h immediately following i.p. injection of 400, 600, or 800 mumol/kg of MA or saline. Feeding was also measured in these rats in response to 2-deoxy-D-glucose (2DG) (100, 200, and 300 mg/kg, SC), a glucose analogue that competitively inhibits glucose utilization. We found that CNA lesions blocked feeding in response to all three doses of MA. Feeding in response to 2DG was significantly reduced, but not abolished, by the lesion. These findings suggest that the CNA is a crucial component of the neural pathway for feeding in response to MA and may also participate in 2DG-induced feeding.