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.
Ferry
B
B
Center for the Neurobiology of Learning and Memory and Department of Neurobiology and Behavior, University of California, Irvine 92697-3800, USA. bferry@uci.edu
Roozendaal
B
B
McGaugh
J L
JL
D058668:Adrenergic alpha-1 Receptor Antagonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001362:Avoidance Learning / Q000187:drug effects; D008297:Male; D008568:Memory / Q000187:drug effects / Q000502:physiology*; D010656:Phenylephrine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology; D015016:Yohimbine / Q000494:pharmacology
D058668:Adrenergic alpha-1 Receptor Antagonists; D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D018340:Receptors, Adrenergic, alpha-1; D011943:Receptors, Adrenergic, beta; D010656:Phenylephrine; D015016:Yohimbine; D001262:Atenolol; D011224:Prazosin