Long term destruction of the tuberoinfundibular dopaminergic neurons results in increased responsiveness of the anterior pituitary to the suppression of PRL release by dopamine. In the present study we tested whether long term destruction of these neurons by medial basal hypothalamic lesions would also increase the potency of dopamine in suppressing the release and apparent synthesis of PRL. Anterior pituitaries from ovariectomized control rats and ovariectomized rats lesioned for 2 weeks were incubated for 3 h in medium 199 containing [3H]leucine in the presence or absence of various concentrations of dopamine. Labeled PRL was separated by polyacrylamide gel electrophoresis and quantitated by liquid scintillation spectroscopy. Concentrations of dopamine ranging from 10-8-10-6B M caused a dose-dependent suppression of labeled newly synthesized PRL released into the medium from anterior pituitaries of medial basal hypothalamus-lesioned animals. With pituitaries from the nonl esioned rats, newly synthesized PRL release was progressively inhibited by 10-7 and 10-6 M dopamine, while 10-8H M dopamine actually significantly stimulated PRL release. Total labeled PRL (that released and that remaining in the gland) was equally suppressed by all three concentrations of dopamine in pituitaries from lesioned animals, but only a minor effect was observed at the highest concentration of dopamine with the control pituitaries. Therefore, the potency of dopamine to suppress the release and apparent synthesis (total labeled PRL) of newly synthesized PRL from pituitaries of long term lesioned animals was increased.
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