Neuroscience 2002 Abstract
| Presentation Number: | 223.5 |
|---|---|
| Abstract Title: | CHRONIC COLD STRESS RESTORES NORADRENERGIC FACILITATION OF THE HPA RESPONSE IN BSTL OF WKY RATS. |
| Authors: |
Morilak, D. A.*1
; Pardon, M. C.1
; Price, D. A.1
1Pharmacol, UTHSC, San Antonio, TX |
| Primary Theme and Topics |
Autonomic, Limbic and Other Systems - Stress and the Brain -- Stress-modulated pathways |
| Secondary Theme and Topics | Autonomic, Limbic and Other Systems<br />- Stress and the Brain<br />-- HPA axis |
| Session: |
223. Stress and the brain Slide |
| Presentation Time: | Monday, November 4, 2002 9:00 AM-9:15 AM |
| Location: | Room 208C |
| Keywords: | norepinephrine, Post-traumatic stress disorder, bed nucleus of stria terminalis, Stress |
We showed that norepinephrine (NE) in the bed nucleus of the stria terminalis (BSTL) facilitates stress-activation of the HPA axis (Cecchi, 2002). We also showed that, despite enhanced HPA responses, activation of the NE system is deficient in WKY compared to Sprague-Dawley (SD) rats. Chronic intermittent cold stress potentiated both HPA activation and stress-induced NE release in BSTL of WKY rats (Pardon, SFN 2001). Here, we examined the degree to which NE contributes to the elevated HPA response of WKY rats, and what effect sensitization of stress-induced NE release by cold stress has on that response. Adult male SD and WKY rats were implanted with jugular catheters and guide cannulae aimed at BSTL. Half of each strain were exposed to 7 days cold stress (4 hr/day, 4 °C). On the test day, vehicle or the α1-antagonist benoxathian (BNX, 2 nmole/0.2 μl) were injected into BSTL before 30 min acute immobilization stress (n=8-13/group). Repeated blood samples were taken to measure plasma ACTH. In control rats, BNX in BSTL attenuated stress-induced ACTH secretion in SD but not WKY rats (p<0.05). After chronic cold exposure, the acute ACTH response was enhanced in both strains. However, in this condition, the HPA response to acute immobilization stress was also attenuated by BNX in both strains (p<0.05), such that the response of WKY rats was no different from that of SD. Thus, chronic cold not only sensitized previously-deficient NE release, but restored noradrenergic facilitation of the already-elevated HPA response in WKY rats. This may be one mechanism whereby exposure to severe or chronic stress may induce pathologic dysregulation of the stress response in genetically susceptible individuals.
Supported by NIMH 53851
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2002 Neuroscience Meeting Planner. Orlando, FL: Society for Neuroscience, 2002. Online.
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