Glucocorticoid receptor activation in the rat nucleus of the solitary tract facilitates memory consolidation: involvement of the basolateral amygdala

These experiments examined the involvement of glucocorticoid receptors (GRs or type II) located in the A2-noradrenergic cell group of the rat nucleus of the solitary tract (NTS) in modulating memory storage. Bilateral intra-N TS infusions (0.5 mu L) of the specific GR agonist RU 28362 (11 beta, 17 be ta-dihydroxy-6,21 -dimethyl-17 alpha-pregna-4,6-trien-20yn-3-one), in doses ranging from 0.01 to 10.0 ng, immediately after inhibitory avoidance train ing produced a dose-dependent enhancement of 48 h retention performance, In fusions of 0.1 or 1.0 ng of the agonist enhanced retention, whereas lower o r higher doses were ineffective. Post-training infusions of the GR antagoni st RU 38486 [17 beta-hydroxy-11 beta-(4-dimethylaminophenyl)-17 alpha-(1 -p ropynyl)-oestra-4,9-dien-3-one, 0.01-10.0 ng] into the NTS did not signific antly affect retention performance, but shifted the dose-response effects o f post-training systemic injections of the synthetic glucocorticoid dexamet hasone to the right. These results indicate that activation of GRs in the N TS can influence memory formation for inhibitory avoidance training, and su ggest that the effects of circulating glucocorticoids on memory are mediate d, in part, by an activation of GRs in the NTS, Additionally, pretraining i nfusions of the beta(1)-adrenergic antagonist atenolol (0.5 mu g in 0.2 mu L) into the basolateral nucleus of the amygdala (BLA), a brain structure wh ich receives noradrenergic projections from the NTS and is implicated in me mory storage modulation, blocked the memory-enhancing effects of the GR ago nist (1.0 ng) infused into the NTS. These findings provide evidence that me mory storage is modulated by glucocorticoid binding to GRs in noradrenergic cell bodies in the NTS and suggest that these modulatory effects are conve yed by ascending projections to the BLA.