Amygdala beta-noradrenergic influences on memory storage involve cholinergic activation

These experiments examined the involvement of the amygdaloid complex as a site of interaction of adrenergic and muscarinic cholinergic influences on memory storage. Male Sprague-Dawley rats (60 days old; 250-300 g) were given a single training trial in an inhibitory avoidance task and a retention test trial 48 h later. Immediately after training buffer control or drug solutions (0.5 mu l) were infused into the amygdala and, in the first experiment only, other drugs were administered intraperitoneally (ip). The first experiment examined the effects of post-training systemic injections of the muscarinic agonist oxotremorine (100.0 mu g/kg) administered alone or together with intra-amygdala injections of either the muscarinic antagonist atropine (1.0 mu g) or the beta-noradrenergic antagonist propranolol (0.3 mu g). Oxotremorine enhanced retention and atropine, but not propranolol, attenuated the effects of oxotremorine. In the second experiment intraamygdala infusions of the beta-noradrenergic agonist clenbuterol (10.0 ng) were administered either alone or together with atropine (1.0 mu g). Clenbuterol enhanced retention and atropine blocked the effects of clenbuterol. In the third experiment intraamygdala infusions of oxotremorine (3, 10, 30, or 100 ng) were administered either alone or together with propranolol(0.3 mu g). Oxotremorine (3.0 and 10.0 ng) enhanced retention and propranolol did not block the effects of oxotremorine. These findings are consistent with the view that memory storage is regulated by an interaction of beta-noradrenergic and cholinergic influences and suggest that the noradrenergic influences are mediated by the release of acetylcholine and activation of muscarinic cholinergic receptors within the amygdala. (C) 1996 Academic Press, Inc.