POSSIBLE INVOLVEMENT OF NITRIC-OXIDE IN RED NUCLEUS STIMULATION-INDUCED ANALGESIA IN THE RAT

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 mu mol), but not of D-arginine, produced quick and long-lasting analgesia. Pretreatment with N-nitro-L-arginine methyl ester (1 mu mol), 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.