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

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 mu g 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 mu g) did not reverse the propranolol-induced inhibitory avoidance deficits. However, coadministration of 2.5 mu g 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.