Inhibitory avoidance impairments induced by intra-amygdala propranolol are reversed by glutamate but not glucose

Abstract

Both systemic and central injections of glucose can enhance memory. For example, glucose reverses impairments on inhibitory avoidance resulting from intra-amygdala injections of morphine. The present experiment investigated the ability of glucose to reverse memory impairments resulting from intra-amygdala injections of propranolol, a beta-noradrenergic antagonist. Pretraining administration of 10 microg propranolol significantly reduced inhibitory avoidance retention latencies but had no effect on performance in a spontaneous alternation task. Coadministration of glucose into the amygdala at 3 doses (1.5, 3.0, and 6.0 microg) did not reverse the propranolol-induced inhibitory avoidance deficits. However, coadministration of 2.5 microg of glutamate with the propranolol did reverse these deficits. The ability of glucose to reverse impairments following intra-amygdala injections of morphine but not propranolol may reflect the neurotransmitter system or systems through which glucose exerts its effects.