Abstract

The present study was designed to elucidate the role of the amygdala as a site of action of muscarinic and nicotinic receptor active drugs in modulating avoidance (passive avoidance) and spatial navigation (water maze) performance. Quisqualic acid lesioning of the nucleus basalis decreased choline acetyltransferase activity in the amygdala and dorsolateral frontal cortex, but not in the hippocampus. Single or combined amygdala and nucleus basalis lesions did not impair water maze navigation. 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 cholinergic antagonists on passive avoidance performance were smaller in amygdala-lesioned rats than in the controls. Amygdala lesions did not modulate the effect of the cholinergic antagonists in impairing water-maze performance. Nicotine, a nicotinic agonist, and arecoline, a muscarinic agonist, restored passive avoidance performance in nucleus basalis-lesioned but not in nucleus basalis+amygdala-lesioned rats. Nicotine and arecoline did not improve water maze navigation in nucleus basalis-lesioned or nucleus basalis+amygdala-lesioned rats. The present results suggest that the nucleus basalis cholinergic projection may modulate passive avoidance performance via amygdaloid muscarinic and nicotinic receptors.