Electrophysiological evidence for a role of nitric oxide in prolonged chemical nociception in the rat

J.E. Haley, A.H. Dickenson, M. Schachter

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

The role of nitric oxide in the periphery and the spinal cord, during acute electrically-evoked and prolonged chemically-evoked nociceptive stimulation, was investigated in rats anaesthetised with halothane. The responses of single dorsal horn neurones to electrically-evoked Aβ fibre and C fibre inputs were reduced by topical application (directly onto the spinal cord) of both the nitric oxide inhibitor, nitro-L-arginine methyl ester (L-NAME; 500-1500 μg) and the precursor of nitric oxide, L-arginine (4500 μg). Administration of L-NAME, either directly into the receptive held (500-1500 μg) or intravenously (10-100 mg/kg) had little or no effect on the acute electrically-evoked activity. Intravenous injection of L-NAME, administered 40 min prior to injection of formalin, significantly reduced the prolonged second peak of firing, with only a small effect on the short-duration first peak. Administration of L-NAME, directly into the site of injection of formalin, as a 10 min pretreatment, significantly reduced the second but not the first peak of the response. Topical application of L-NAME onto the spinal cord, as a 30 min pretreatment, significantly reduced both the first and second peaks of the response. This inhibition was not reversed by the coadministration of L-arginine, which was inhibitory by itself. Thus, nitric oxide may be involved, in a complex way, in nociceptive events both in the periphery and within the spinal cord.
Original languageEnglish
Pages (from-to)251-258
Number of pages8
JournalNeuropharmacology
Volume31
Issue number3
DOIs
Publication statusPublished - 1 Jan 1992

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