Ethanol dose-dependently attenuates NMDA-mediated thermal hyperalgesia in the rat.
Recent observations using acute and persistent pain models have suggested that activation of the N-methyl-D-aspartate (NMDA) receptor is required for mechanisms that underly the development and maintenance of thermal hyperalgesia. The present results document that both NMDA-mediated thermal hyperalgesia produced after acute intrathecal NMDA administration and NMDA-mediated thermal hyperalgesia produced in a model of neuropathic pain are dose-dependently and reversibly attenuated by intrathecal administration of ethanol (0.5-1.0%; total dose, 106-213 nmol, i.t.). This is consistent with recent reports that ethanol may function as a selective NMDA receptor antagonist at low concentrations and further extends the evidence that thermal hyperalgesia is mediated by NMDA receptors.
Meller
S T
ST
Department of Pharmacology, University of Iowa, Iowa City 52242.
Dykstra
C
C
Pechman
P S
PS
Maves
T J
TJ
Gebhart
G F
GF
D000818:Animals; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000494:pharmacology*; D006358:Hot Temperature; D007278:Injections, Spinal; D008297:Male; D016202:N-Methylaspartate / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000494:pharmacology; D010146:Pain / Q000503:physiopathology*; D010147:Pain Measurement / Q000187:drug effects; D017288:Pain Threshold / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000502:physiology*; D012018:Reflex / Q000187:drug effects
D016194:Receptors, N-Methyl-D-Aspartate; D000431:Ethanol; D016202:N-Methylaspartate