Abstract
There is considerable evidence that nitric oxide (NO) plays a role in synaptic transmission in both central and peripheral nervous systems. Recent studies have suggested the involvement of the l-arginine-NO pathway in nociceptive transmission/modulation. Electrical stimulation of the red nucleus in the rat evokes potent analgesia. Microinjection of different concentrations of l-arginine (1 nmol–1 μmol), but not of d-arginine, produced quick and long-lasting analgesia. Pretreatment with N-nitro- l-arginine methyl ester (1 μmol), a nitric oxide synthase inhibitor, significantly prevented l-arginine-induced analgesia. Further, pretreatment of animals with methylene blue, a known guanylate cyclase inhibitor, also attenuated the development of analgesia. Our results suggest that l-arginine caused production of NO, which in turn activated the red nucleus analgesic system.
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