CHOLINERGIC DRUGS REGULATE PASSIVE-AVOIDANCE PERFORMANCE VIA THE AMYGDALA

The present study was designed to elucidate the role of the amygdala a s a site of action of muscarinic and nicotinic receptor active drugs i n modulating avoidance (passive avoidance) and spatial navigation (wat er maze) performance. Quisqualic acid lesioning of the nucleus basalis decreased choline acetyltransferase activity in the amygdala and dors olateral frontal cortex, but not in the hippocampus. Single or combine d amygdala and nucleus basalis lesions did not impair water maze navig ation. Combined amygdala and nucleus basalis lesioning did not impair passive avoidance performance any more severely than did either of the lesions alone. Scopolamine (a muscarinic antagonist) and mecamylamine (a nicotinic antagonist) induced a dose-dependent impairment of both passive avoidance and water maze performance. The effects of the choli nergic antagonists on passive avoidance performance were smaller in am ygdala-lesioned rats than in the controls. Amygdala lesions did not mo dulate the effect of the cholinergic antagonists in impairing water-ma ze performance. Nicotine, a nicotinic agonist, and arecoline, a muscar inic agonist, restored passive avoidance performance in nucleus basali s-lesioned but not in nucleus basalis + amygdala-lesioned rats. Nicoti ne and arecoline did not improve water maze navigation in nucleus basa lis-lesioned or nucleus basalis + amygdala-lesioned rats. The present results suggest that the nucleus basalis cholinergic projection may mo dulate passive avoidance performance via amygdaloid muscarinic and nic otinic receptors.