Journal
NEUROSCIENCE
Volume 138, Issue 3, Pages 901-910Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2005.07.049
Keywords
amygdala; corticosterone; emotional arousal; memory consolidation; memory retrieval; working memory
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Funding
- NIMH NIH HHS [MH12526] Funding Source: Medline
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH012526, R37MH012526, R56MH012526] Funding Source: NIH RePORTER
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Extensive evidence from rat and human studies indicates that glucocorticoid hormones influence cognitive performance. Posttraining activation of glucocorticoid-sensitive pathways dose-dependently enhances the consolidation of long-term memory. Glucocorticoid effects on memory consolidation rely on noradrenergic activation of the basolateral amygdala and interactions of the basolateral amygdala with other brain regions. Glucocorticolds interact with the noradrenergic system both at a postsynaptic level, increasing the efficacy of the beta-adrenoceptor-cyclic AMP/protein kinase A system, as well as presynaptically in brainstem noradrenergic cell groups that project to the basolateral amygdala. In contrast, memory retrieval and working memory performance are impaired with high circulating levels of glucocorticoids. Glucocorticoid-induced impairment of these two memory functions also requires the integrity of the basolateral amygdala and the noradrenergic system. Such critical interactions between glucocorticoids and noradrenergic activation of the basolateral amygdala have important consequences for the role of emotional arousal in enabling glucocorticoid effects on these different memory functions. (C) 2005 Published by Elsevier Ltd on behalf of IBRO.
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