Journal
JOURNAL OF NEUROSCIENCE
Volume 24, Issue 6, Pages 1385-1392Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4664-03.2004
Keywords
beta-adrenoceptor; corticosterone; delayed alternation task; glucocorticoid receptor; norepinephrine; propranolol; RU 28362; stress hormone
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Funding
- NIMH NIH HHS [MH12526, R56 MH012526, R01 MH012526] Funding Source: Medline
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Previous findings indicate that the basolateral complex of the amygdala (BLA) interacts with other brain regions in regulating stress hormone effects on memory functions. Lesions of the BLA or infusions of a beta-adrenoceptor antagonist into the BLA block glucocorticoid effects on both memory consolidation and retrieval when administered either systemically or directly into the hippocampus. The present experiments examined BLA and beta-adrenoceptor involvement in regulating glucocorticoid effects on spatial working memory, a task that depends on the medial prefrontal cortex (mPFC). Male Sprague Dawley rats with bilateral sham- or NMDA-induced lesions of the BLA received either corticosterone (1.0 or 3.0 mg/kg, i.p.) systemically or the specific glucocorticoid receptor agonist 11beta, 17beta-dihydroxy-6,21- dimethyl-17alpha-pregna-4,6-trien-20yn-3-one (RU 28362; 3.0 or 10.0 ng in 0.5 mul) into the mPFC shortly before testing on a delayed alternation task in a T-maze. Both glucocorticoid treatments induced comparable impairments in working memory performance in sham- lesioned controls. Although lesions of the BLA alone did not affect working memory, BLA lesions blocked the impairment induced by either corticosterone or RU 28362. Likewise, systemic injections of the centrally acting beta-adrenoceptor antagonist propranolol (2.0 mg/kg, i.p.) given before testing prevented corticosterone-induced working memory impairment. These findings indicate that BLA activity is essential for enabling glucocorticoid effects in the mPFC on working memory and suggest that stress hormone-induced modulation of working memory involves noradrenergic activation.
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