Involvement of alpha1-adrenoceptors in the basolateral amygdala in modulation of memory storage.

These experiments examined the involvement of alpha1-adrenoceptors in the basolateral amygdala and their interaction with beta-adrenoceptors in modulating memory storage. In Experiment 1, male Sprague-Dawley rats, implanted with bilateral cannulae in the basolateral amygdala, were trained in a one-trial inhibitory avoidance task and immediately after training, were given microinfusions (0.2 microl/side) of the selective alpha1-adrenoceptor antagonist, prazosin (0.1-1.0 microg). Retention was tested 48 h later. Prazosin induced a dose-dependent impairment in retention performance. In Experiment 2, animals received post-training intra-basolateral amygdala infusions of phenylephrine (a non-selective alpha-adrenoceptor agonist; 1.0-10.0 microg) alone or in combination with yohimbine (a selective alpha2-adrenoceptor antagonist; 0.2 microg) to examine the effects, on memory storage, of selective alpha1-adrenoceptor activation. Low doses of phenylephrine alone tended to impair retention performance, whereas the highest dose was non-effective. In contrast, phenylephrine infused together with yohimbine induced a dose-dependent enhancement of retention performance, suggesting that a selective activation of alpha1-adrenoceptors enhances memory formation. In Experiment 3, animals received intra-basolateral amygdala infusions of phenylephrine (1.0-10.0 microg) and yohimbine (0.2 microg) in combination with atenolol (a beta1-adrenoceptor antagonist; 1.0 microg). Atenolol blocked the memory-enhancing effects induced by infusions of phenylephrine together with yohimbine. Considered together, these findings suggest that alpha1-adrenoceptors in the basolateral amygdala are implicated in mediating the effects of norepinephrine on memory storage and that their action depends on concurrent beta-adrenoceptor activation.