Production of endogenous nitric oxide and activation of soluble guanylate cyclase are required for N-methyl-D-aspartate-produced facilitation of the nociceptive tail-flick reflex
- 7 April 1992
- journal article
- research article
- Published by Elsevier in European Journal of Pharmacology
- Vol. 214 (1) , 93-96
- https://doi.org/10.1016/0014-2999(92)90102-a
Abstract
No abstract availableKeywords
This publication has 8 references indexed in Scilit:
- MK-801 blocks the development of thermal hyperalgesia in a rat model of experimental painful neuropathyBrain Research, 1991
- The induction and maintenance of central sensitization is dependent onN-methyl-d-aspartic acid receptor activation; implications for the treatment of post-injury pain hypersensitivity statesPublished by Wolters Kluwer Health ,1991
- Antagonism at the glycine site on the NMDA receptor reduces spinal nociception in the ratNeuroscience Letters, 1991
- l‐NG‐nitro arginine methyl ester exhibits antinociceptive activity in the mouseBritish Journal of Pharmacology, 1991
- Peripheral analgesia and activation of the nitric oxide-cyclic GMP pathwayEuropean Journal of Pharmacology, 1990
- Endothelium-derived relaxing factor release on activation of NMDA receptors suggests role as intercellular messenger in the brainNature, 1988
- IntrathecalN-methyl-d-aspartate (NMDA) activates both nociceptive and antinociceptive systemsBrain Research, 1987
- The behavioural effects of an N-methylaspartate receptor antagonist following application to the lumbar spinal cord of conscious ratsNeuropharmacology, 1984