Glutamate-induced analgesia: blockade and potentiation by naloxone.
Injection of 0.5 microliter L-sodium glutamate (60 mM) into the periaqueductal gray matter of the rat resulted in a short-lived analgesia as assessed by the tail-flick method. Naloxone (1 mg/kg) attenuated glutamate-induced analgesia when injected 30 min but not 5 min before testing. Paradoxically, a higher dose of naloxone (10 mg/kg) significantly potentiated glutamate analgesia when injected 5 min but not 30 min before testing. Moreover, this higher dose also potentiated analgesia when injected 5 min prior to 12 mM glutamate, a dose of glutamate previously found to be ineffective in causing analgesia. Microinjections of either 60 mM or 1 M KCl failed to elicit analgesia, indicating the specificity of the glutamate effect. Taken together with several other lines of evidence, the present findings suggest that glutamate-induced analgesia may be mediated by processes quite different from those underlying morphine analgesia. It is further suggested that a dose-related naloxone antagonism is not a necessary criterion for assessing endogenous opioid activity.
D000818:Animals; D004305:Dose-Response Relationship, Drug; D005971:Glutamates / Q000494:pharmacology*; D008297:Male; D008636:Mesencephalon / Q000187:drug effects*; D009270:Naloxone / Q000494:pharmacology*; D009619:Nociceptors / Q000187:drug effects*; D051381:Rats
D005971:Glutamates; D009270:Naloxone