NO EVIDENCE FOR CONTRIBUTION OF NITRIC-OXIDE TO SPINAL REFLEX ACTIVITY IN THE RAT SPINAL-CORD IN-VITRO

The effects of nitric oxide (NO) synthase inhibition, NO generation and an N-methyl-D-aspartic acid (NMDA) receptor antagonist upon spinal reflex responses evoked by electrical activation of high threshold afferent fibres and brief application of NMDA have been compared in an in vitro preparation of the neonatal rat spinal cord. Reflex responses of spinal cords prepared from naive animals and those exhibiting a behavioural hyperreflexia following UV irradiation of the left hindpaw have been compared. C-fibre evoked and NMDA induced ventral root potential responses were significantly reduced by the selective NMDA receptor antagonist D-AP5 (40 mu M) but completely unaffected by application of 7-nitroindazole (30 mu M), N-G-nitro-L-arginine methyl ester (L-NAME; 100 mu M) or sodium nitroprusside (50 mu M) either in hyperalgesic or naive animals. In vivo behavioural experiments performed upon age-matched rat pups showed that reflex sensitivity was significantly reduced following administration of L-NAME (30 mg kg(-1)). The present study has failed to provide evidence that NO is involved in nociceptive spinal reflex activity measured in vitro. In contrast, an NO synthase inhibitor was shown to influence nociceptive reflex responses observed in vivo. We suggest it is possible that NO participates in post injury induced hyperreflexia at sites other than directly upon spinal neurones.