Basolateral Amygdala Noradrenergic Influences on Memory Storage Are Mediated by an Interaction between β- and α1-Adrenoceptors

Extensive evidence indicates that norepinephrine modulates memory storage through an activation of β-adrenoceptors in the basolateral nucleus of the amygdala (BLA). Recent findings suggest that the effects of β-adrenergic activation on memory storage are influenced by α1-adrenoceptor stimulation. Pharmacological findings indicate that activation of postsynaptic α1-adrenoceptors potentiates β-adrenoceptor-mediated activation of cAMP formation. The present study examined whether inactivation of α1-adrenoceptors in the BLA would alter the dose–response effects on memory storage of intra-BLA infusions of a β-adrenoceptor agonist, as well as that of a synthetic cAMP analog. Male Sprague Dawley rats received bilateral microinfusions into the BLA of either the β-adrenoceptor agonist clenbuterol (3–3000 pmol in 0.2 μl) or 8-bromoadenosine 3′:5′-cyclic monophosphate (8-bromo-cAMP) (0.2–7 nmol in 0.2 μl) alone or together with the α1-adrenoceptor antagonist prazosin (0.2 nmol) immediately after training in an inhibitory avoidance task. Retention was tested 48 hr later. Clenbuterol induced a dose-dependent enhancement of retention, and prazosin attenuated the dose–response effects of clenbuterol. Posttraining intra-BLA infusions of 8-bromo-cAMP also induced a dose-dependent enhancement of retention latencies. However, concurrent infusion of prazosin did not alter the dose–response effects of 8-bromo-cAMP. These findings are consistent with the view that α1-adrenoceptors affect memory storage by modulating β-adrenoceptor activation in the BLA. Moreover, these findings are consistent with those of pharmacological studies indicating that β-adrenoceptors modulate memory storage by a direct coupling to adenylate cyclase, whereas α1-receptors act indirectly by influencing the β-adrenoceptor-mediated influence on cAMP formation.