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Eur J Neurosci. 1997 Jan;9(1):76-83.

Basolateral amygdala lesions block the memory-enhancing effect of glucocorticoid administration in the dorsal hippocampus of rats.

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Center for the Neurobiology of Learning and Memory, University of California, Irvine 92697-3800, USA.


These experiments examined the effects of bilateral amygdala nuclei lesions on modulation of memory storage induced by bilateral intrahippocampal microinfusions of glucocorticoids in male Sprague-Dawley rats. Post-training infusions of the glucocorticoid receptor (type II) agonist RU 28362 (3.0 or 10.0 ng) enhanced inhibitory avoidance retention, and infusions of the glucocorticoid receptor antagonist RU 38486 (3.0 or 10.0 ng) administered shortly before training in a water maze spatial task did not affect acquisition, but imparied retention. In both tasks, neurochemically induced lesions of the basolateral but not of the central amygdala blocked the memory-modulatory effects of the intrahippocampal infusions of the drugs affecting glucocorticoid receptors. Lesions of the central amygdala alone impaired inhibitory avoidance retention, but basolateral amygdala lesions alone did not affect acquisition or retention in either task. These findings are consistent with previous evidence indicating that lesions of the basolateral amygdala block the memory-modulatory effects of systemically administered glucocorticoids, and provide further evidence that the basolateral amygdala is a critical area involved in regulating glucocorticoid effects in other brain regions involved in memory storage.

[Indexed for MEDLINE]

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