INHIBITION OF NITRIC-OXIDE SYNTHASE ENHANCES MORPHINE ANTINOCICEPTION IN THE RAT SPINAL-CORD

N(G)-nitro-L-arginine methyl ester (L-NAME, 400-1500mug) , administered intrathecally (ith.) , elicits a slight but dose-related antinociception in rats, assessed by tail-flick and paw pressure tests. L-NAME (400mug) and morphine (0.5mug) coadministered ith. elicit a profound and long-lasting antinociception, which is abolished by ith. administration of 3-morpholino-sydnonimine (SIN-1, 100mug) . Hemoglobin (266mug) administered ith. also slightly potentiates morphine antinociception. These results suggest that nitric oxide (NO) is involved in spinal nociceptive events, and that the increased production of No following the nociceptive input may diminish the efficiency of opioid antinociception in the spinal cord.