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 th e basolateral (BLA), central (CEA), or medial amygdala (MEA) were trai ned in a one-trial inhibitory avoidance task. Systemic (sc) injections of either vehicle, corticosterone (0.3 mg/kg) or the more selective g lucocorticoid receptor (GR) agonist dexamethasone (0.3 mg/kg) were adm inistered immediately after training, and retention was tested 48 h la ter. Retention of animals with lesions of the CEA was impaired, but re tention of animals with BLA or MEA lesions was unimpaired. CEA-lesione d animals had increased locomotor activity as indicated by the number of crossings between the starting and shock compartments. Dexamethason e enhanced retention in sham-operated controls as well as in animals w ith lesions of the CEA, but did not enhance retention of animals with BLA or MEA lesions. Post-training corticosterone did not affect retent ion. Neither dexamethasone nor corticosterone altered the number of cr ossings between compartments. These findings are consistent with previ ous evidence suggesting that the effects of glucocorticoids on memory storage are mediated by an activation of GRs, and indicate that the BL A and MEA nuclei are critical areas involved in integrating these horm onal influences on learning and memory. (C) 1996 Academic Press, Inc.