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1 Department of Medicine, Center for Neurovisceral Sciences & Women's Health, Los Angeles, CA, USA
2 Department of Medicine, Center for Neurovisceral Sciences & Women's Health, Los Angeles, CA, USA; VA GLAHS - West Los Angeles Healthcare Center, Center for Neurovisceral Sciences & Women's Health, Los Angeles, CA, USA
3 Department of Medicine, Center for Neurovisceral Sciences & Women's Health, Los Angeles, CA, USA; Department of Physiology, Center for Neurovisceral Sciences & Women's Health, Los Angeles, CA, USA; Department of Psychiatry & Behavioral Sciences, Center for Neurovisceral Sciences & Women's Health, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: emayer{at}ucla.edu.
The mechanism(s) underlying stress-induced colonic hypersensitivity (SICH) are incompletely understood. Our aims were to assess the acute and delayed (24 h) effect of water avoidance (WA) stress on visceral nociception in awake male Wistar rats and to evaluate the role of two stress-related modulation systems: the substance P/neurokinin-1 receptor (SP/NK1R) and the corticotropin-releasing factor (CRF)/CRF1 receptor (CRF/CRF1R) systems, as well as the possible involvement of the sympathetic nervous system (SNS). Visceral pain responses were measured as the visceromotor response (VMR) to colorectal distension (CRD) at baseline, immediately after WA and again 24 h later. The NK1R antagonists RP67580 and SR140333 and the CRF1R antagonist CP154526 were injected 15 min before WA or 1 h before the CRD on day 2. Chemical sympathectomy was performed by repeated injection of 6-hydroxy-dopamine. WA stress resulted in a significant increase in the VMR on day 2, but no change immediately after WA. Injection of CP154526 abolished delayed SICH when applied either before WA stress or before the CRD on day 2. Both NK1R antagonists only decreased SICH when injected before the CRD on day 2. Chemical sympathectomy did not affect delayed SICH. Our results indicate that in male Wistar rats, both NK1R and CRF1R activation, but not SNS activation, play a role in the development of SICH.
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