Journal
PSYCHONEUROENDOCRINOLOGY
Volume 33, Issue 5, Pages 659-669Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.psyneuen.2008.02.006
Keywords
BST; corticotropin releasing hormone; vasopressin; paraventricular nucleus of the hypothalamus; corticosterone; ACTH
Categories
Funding
- NIDA NIH HHS [F32 DA016466, DA16466] Funding Source: Medline
- NIDDK NIH HHS [DK67820, DK59803, F32 DK067820, T32 DK059803] Funding Source: Medline
- NIMH NIH HHS [MH49698, R01 MH069725, R01 MH049698] Funding Source: Medline
- NINDS NIH HHS [NS07453, T32 NS007453] Funding Source: Medline
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The bed nucleus of the stria terminalis (BST) plays a prominent role in brain integration of acute responses to stressful stimuli. This study tests the hypothesis that the BST plays a complementary rote in regulation of physiological changes associated with chronic stress exposure. Mate Sprague-Dawley rats received bilateral ibotenate lesions or sham lesions of the posterior medial region of the BST (BSTpm), an area known to be involved in inhibition of HPA axis responses to acute stress. Chronic stress was induced by 14-day exposure to twice daily stressors in an unpredictable sequence (chronic variable stress, CVS). In the morning after the end of CVS, stressed and non-stressed controls were exposed to a novel restraint stress challenge. As previously documented, CVS caused adrenal hypertrophy, thymic involution, and attenuated body weight gain. None of these endpoints were affected by BSTpm lesions. Chronic stress exposure facilitated plasma corticosterone responses to the novel restraint stress and elevated CRH mRNA. Lesions of the BSTpm increased novel stressor-induced plasma ACTH and corticosterone secretion and enhanced c-fos mRNA induction in the paraventricular nucleus of the hypothalamus (PVN). In addition, lesion of the BSTpm resulted in an additive increase in CVS-induced facilitation of corticosterone responses and PVN CRH expression. Collectively these data confirm that the BSTpm markedly inhibits HPA responses to acute stress, but do not strongly support an additional role for this region in limiting HPA axis responses to chronic drive. The data further suggest that acute versus chronic stress integration are subserved by different brain circuitry. (C) 2008 Published by Elsevier Ltd.
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