Monosodium glutamate and analgesia induced by morphine. Test-specific effects

Diana Badillo-martinez, Annette L. Kirchgessner, Pamela D. Butler, R. J. Bodnar

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


Neonatal administration of monosodium glutamate (MSG) destroyed perikarya in the arcuate nucleus and median eminence, including those that contain met-enkephalin and beta-endorphin and it increased the density of opiate receptors in the midbrain. Treatment with glutamate decreased the analgesic response on the jump test following a 10 mg/kg dose of morphine, yet increased the analgesic response on the hot-plate test following a 1 mg/kg dose of morphine. The present study demonstrated that changes in morphine-induced analgesia induced by glutamate varied as functions of the pain test and of gender. While males treated with glutamate displayed attenuated analgesia induced by morphine (2.5-15 mg/kg) on the jump test, jump thresholds of females treated with glutamate were potentiated after a 10 mg/kg dose of morphine and attenuated after a 15 mg/kg dose of morphine, relative o controls. In contrast, analgesia on the hot-plate test was potentiated in animals of both genders treated with glutamate after all doses of morphine. Changes in tolerance to morphine induced by glutamate also depended on the pain test and gender. While the peak analgesic response on the jump test did not occur until the fifth injection of morphine in all rats treated with glutamate, tolerance on the jump test was subsequently retarded in males treated with glutamate and accelerated in glutamate-treated females. Tolerance on the hot-plate test appeared not to be consistently affected by treatment with glutamate. Morphine-induced hyperthermia was initially decreased in rats treated with glutamate, but subsequently decreased in glutamate-treated males and increased in glutamate-treated females. Loss of body weight induced by the chronic administration of opiates was exacerbated by treatment with glutamate, particularly in males. These data are discussed in terms of other neuroendocrinological dysfunctions induced by neonatal treatment with glutamate and they indicate that no simple model of selective destruction of stores of endogenous opioids can account for all of the alterations in the responses to opiates.

Original languageEnglish
Pages (from-to)1141-1149
Number of pages9
Issue number10
StatePublished - Oct 1984
Externally publishedYes


  • analgesia
  • body weight
  • coping
  • monosodium glutamate
  • morphine
  • rats
  • thermoregulation


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