Glutamate-induced analgesia: Blockade and potentiation by naloxone

Gideon Urca, Richard L. Nahin, John C. Liebeskind*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

68 Scopus citations


Injection of 0.5 μl 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.

Original languageEnglish
Pages (from-to)523-530
Number of pages8
JournalBrain Research
Issue number2
StatePublished - 23 Jun 1980


FundersFunder number
N.I.H.NS 07628


    • analgesia
    • glutamate
    • naloxone
    • periaqueductal gray matter


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