Loss of morphine hyperphagia following neonatal monosodium glutamate treatment in rats.
Morphine stimulates food intake in mildly-deprived and nondeprived rats. Neonatal administration of monosodium glutamate (MSG) destroys the medial-basal hypothalamus and other circumventricular organs, including cells containing beta-endorphin that project to other hypothalamic nuclei proposed in the modulation of morphine hyperphagia. Food intake of MSG-treated and control rats were assessed following vehicle and morphine (1.0-5.0 mg/kg, sc) treatment in a mild (5h) food deprivation paradigm. Morphine hyperphagia was found to be absent in MSG-treated rats, although they responded normally to mild deprivation following vehicle treatment. These results add to the types of ingestive deficits observed in the MSG-treated rat, and suggest that the circumventricular system in general, and opioid medial-basal hypothalamic cells in particular may be implicated in morphine hyperphagia.
D000818:Animals; D001111:Arcuate Nucleus of Hypothalamus / Q000187:drug effects / Q000473:pathology; D004435:Eating / Q000187:drug effects*; D005260:Female; D005508:Food Deprivation; D005971:Glutamates / Q000494:pharmacology*; D007033:Hypothalamus, Middle / Q000187:drug effects / Q000502:physiology; D008473:Median Eminence / Q000187:drug effects / Q000473:pathology; D009020:Morphine / Q000494:pharmacology*; D009336:Necrosis; D051381:Rats; D012970:Sodium Glutamate / Q000494:pharmacology*
D005971:Glutamates; D009020:Morphine; D012970:Sodium Glutamate