Abstract
Several lines of evidence indicate that β-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 β-endorphin. Neonatal treatment with monosodium glutamate (MSG) reduced drastically the content of β-endorphin-like immunoreactivity (β-EI) of hypothalamus but not the β-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 β-endorphin is not involved in the control of vasopressin release during foot shock-induced stress in the rat.
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