Direct and indirect effects of nitric oxide on nociceptive signal transduction at the trigeminal nucleus caudalis and mechanism for the regulation

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Effect of nitric oxide on the transmission of noxious stimuli for trigeminal nerve were investigated, using experimental animals inserted microdialysis probe into the trigeminal nucleus, perfusion of nerve terminal preparation, synaptosomes, from the nucleus, and treatment of cultured human neuroblastoma cells.The stimulation of dental pulp caused release of substance P from region of trigeminal sensory nerve terminals in vivo. The administration with an agent to stimulate glutamate receptors resulted in enhanced production of nitric oxide. Moreover, observed was the interaction of nitric oxide with signal transmission in animals of allodynia, hypersensitive condition.The perfusion experiments of primary afferent nerve terminals with nitric oxide donor indicated that nitric oxide attenuated the depolarization-evoked release of substance P, but not that of glutamate, probably through the mechanism that nitric oxide stimulated guanylate cyclase to produce nitric oxide in nerve terminals.On the other hand, the excess production of nitric oxide may cause cell death through the nitration of adhesion proteins with the elevation of intracellular calcium concentration.In conclusion, the noxious stimuli of maxillofacial regions causes release from primary afferent nerve terminals, and then activation of nitric oxide synthase to produce nitric oxide, that regulates release of substance P in an inhibitory fashion at trigeminal nucleus.