Effect of neonatal treatment with monosodium glutamate on vasopressin release during foot shock stress in the rat.
Several lines of evidence indicate that beta-endorphin inhibits the release of vasopressin during foot shock-induced stress in the rat. This study was to evaluate the relative importance of the hypothalamic versus the pituitary pool of beta-endorphin. Neonatal treatment with monosodium glutamate (MSG) reduced drastically the content of beta-endorphin-like immunoreactivity (beta-EI) of hypothalamus but not the beta-EI concentration in the pituitary; the content of vasopressin in the hypothalamus and the pituitary was not altered by MSG treatment. MSG treatment had no effect on the plasma vasopressin response to inescapable electric foot shock stress, when compared to controls. Naloxone enhanced vasopressin release during stress both in MSG-treated rats and in controls. These results suggest that hypothalamic beta-endorphin is not involved in the control of vasopressin release during foot shock-induced stress in the rat.
D000818:Animals; D000831:Animals, Newborn; D004597:Electroshock; D004723:Endorphins / Q000502:physiology; D005260:Female; D005971:Glutamates / Q000494:pharmacology*; D007031:Hypothalamus / Q000187:drug effects; D009270:Naloxone / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012970:Sodium Glutamate / Q000494:pharmacology*; D013312:Stress, Physiological / Q000378:metabolism*; D014667:Vasopressins / Q000378:metabolism*; D001615:beta-Endorphin
D004723:Endorphins; D005971:Glutamates; D014667:Vasopressins; D009270:Naloxone; D001615:beta-Endorphin; D012970:Sodium Glutamate