Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 429, Issue 1-3, Pages 319-325Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/S0014-2999(01)01331-0
Keywords
inflammation; colorectal distension; NMDA receptor; N-nitro-L-arginine methyl ester (L-NAME); rostral ventromedial medulla
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Funding
- NIDA NIH HHS [DA11431, DA02879] Funding Source: Medline
- NINDS NIH HHS [NS19912] Funding Source: Medline
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The studies summarized here document the role of NMDA receptors and nitric oxide in the lumbosacral spinal cord and rostral ventromedial medulla in the maintenance of visceral hyperalgesia. Experiments were conducted in rats in which drugs were administered into either the lumbosacral intrathecal space or directly into the rostral ventromedial medulla. The visceral stimulus was noxious colorectal distension, administered before and 3 h after intracolonic instillation of either saline or 25% zymosan. The visceromotor response to colonic distension was quantified and found to be significantly enhanced in rats in which the colon had previously been treated with zymosan. Enhanced responses to distension were attenuated dose-dependently by intrathecal administration of the NMA receptor channel blocker MK-801 and by inhibition of the neuronal isoform of nitric oxide synthase (nNOS). In corresponding studies wherein drugs were administered directly into the rostral ventromedial medulla, NMDA receptor antagonism and NOS inhibition dose-dependently attenuated exaggerated responses to colonic distension. Taken together, these data suggest that zymosan-produced visceral hyperalgesia is influenced both at the level of the spinal cord and rostral ventromedial medulla, and that descending facilitatory influences from the rostral ventromedial medulla are important to the maintenance of visceral hyperalgesia. (C) 2001 Elsevier Science B.V. All rights reserved.
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