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Submitted on August 15, 2005
Accepted on December 22, 2005
Department of Psychiatry, University of Cincinnati, Psychiatry Service, Cincinnati Veterans Affairs Medical Center, Cincinnati, OH 45237 USA
* To whom correspondence should be addressed. E-mail: michelle.ostrander{at}uc.edu.
Chronic stress induces both functional and structural adaptations within the hypothalamo-pituitary-adrenocortical (HPA) axis, suggestive of long-term alterations in neuroendocrine reactivity to subsequent stressors. We hypothesized that prior chronic stress would produce persistent enhancement of HPA axis reactivity to novel stressors. Adult male rats were exposed to chronic variable stress (CVS) for one week and allowed to recover. Plasma ACTH and corticosterone levels were measured in control or CVS rats exposed to novel psychogenic (novel environment or restraint) or systemic (hypoxia) stressors at 16 h, 4 d, 7 d, or 30 d after CVS cessation. Plasma ACTH and corticosterone responses to psychogenic stressors were attenuated at 4 d (novel environment and restraint) and 7 d (novel environment only) recovery from CVS, while hormonal responses to the systemic stressor were largely unaffected by CVS. CRH (CRH) mRNA expression was up-regulated in the paraventricular nucleus of the hypothalamus (PVN) at 16 h following cessation of CVS, but no other alterations in PVN CRH or arginine vasopressin (AVP) mRNA expression were observed. Thus, in contrast to our hypothesis, reductions of HPA axis sensitivity to psychogenic stressors manifested at delayed recovery time points following CVS. The capacity of the HPA axis to respond to a systemic stressor appeared largely intact during recovery from CVS. These data suggest that chronic stress selectively targets brain circuits responsible for integration of psychogenic stimuli, resulting in decreased HPA axis responsiveness possibly mediated in part by transitory alterations in PVN CRH expression.
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