Hyperalgesia mediated by spinal glutamate or substance P receptor blocked by spinal cyclooxygenase inhibition.

Article date: 1992/8/28

PubMed ID: 1381521

Journal name: Science (New York, N.Y.) (ISSN: 0036-8075)


Inhibition of cyclooxygenase by nonsteroidal anti-inflammatory drugs (NSAIDs) in the periphery is commonly accepted as the primary mechanism by which these agents produce a selective attenuation of pain (analgesia). NSAIDs are now shown to exert a direct spinal action by blocking the excessive sensitivity to pain (hyperalgesia) induced by the activation of spinal glutamate and substance P receptors. These findings demonstrate that the analgesic effects of NSAIDs can be dissociated from their anti-inflammatory actions. Spinal prostanoids are thus critical for the augmented processing of pain information at the spinal level.

Author List: Malmberg A B, Yaksh T L

Publication Types: Journal Article; Research Support, U.S. Gov't, P.H.S.

Substances mentioned in the article: Glutamates; Quinoxalines; Receptors, Neurokinin-1; Receptors, Neurotransmitter; Receptors, Tachykinin; Ibotenic Acid; Substance P; Glutamic Acid; N-Methylaspartate; Dizocilpine Maleate; 6-Cyano-7-nitroquinoxaline-2,3-dione; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Prostaglandin-Endoperoxide Synthases;

Mesh terms: 6-Cyano-7-nitroquinoxaline-2,3-dione; Dizocilpine Maleate/pharmacology; Dose-Response Relationship, Drug; Glutamates/physiology; Glutamic Acid; Hyperalgesia/drug therapy; Ibotenic Acid/analogs & derivatives; Injections, Spinal; N-Methylaspartate/pharmacology; Prostaglandin-Endoperoxide Synthases/physiology; Quinoxalines/pharmacology; Receptors, Neurokinin-1; Receptors, Neurotransmitter/physiology; Receptors, Tachykinin; Substance P/pharmacology; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid;

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