Amygdaloid nuclei lesions differentially affect glucocorticoid-induced memory enhancement in an inhibitory avoidance task.

This study examined the involvement of the amygdala in the effects of glucocorticoids on the formation of memory for aversive training. Male Sprague-Dawley rats with neurochemically induced lesions of either the basolateral (BLA), central (CEA), or medial amygdala (MEA) were trained in a one-trial inhibitory avoidance task. Systemic (sc) injections of either vehicle, corticosterone (0.3 mg/kg) or the more selective glucocorticoid receptor (GR) agonist dexamethasone (0.3 mg/kg) were administered immediately after training, and retention was tested 48 h later. Retention of animals with lesions of the CEA was impaired, but retention of animals with BLA or MEA lesions was unimpaired. CEA-lesioned animals had increased locomotor activity as indicated by the number of crossings between the starting and shock compartments. Dexamethasone enhanced retention in sham-operated controls as well as in animals with lesions of the CEA, but did not enhance retention of animals with BLA or MEA lesions. Post-training corticosterone did not affect retention. Neither dexamethasone nor corticosterone altered the number of crossings between compartments. These findings are consistent with previous evidence suggesting that the effects of glucocorticoids on memory storage are mediated by an activation of GRs, and indicate that the BLA and MEA nuclei are critical areas involved in integrating these hormonal influences on learning and memory.