In ovariectomized, estrogen-treated rats (10 μg estradiol benzoate (Eb), SC, 48 hr before) bearing a permanent cannula in the third ventricle (3rd V), the third ventricular injection of dopamine (DA) (2 μg), but not of norepinephrine (NE) (2 μg) or of physiological saline solution (4 μl) decreased plasma prolactin titers 15 and 30 min after the injection. Apomorphine (A) (4, 20 or 40 μg in 4 μl) dramatically drecreased prolactin 15, 30 and 60 min later. Dibutyryl cyclic AMP (DBC) (93.6 μg; 0.05M, 4 μl) but not 5′ AMP (68.4 μg, 0.05M) mimicked the effect of DA and A. In ovariectomized rats, Pimozide (0.63 mg/kg), a dopaminergic receptor blocker, injected SC 1 hr before prevented the effect of DA but not that of DBC. Prostaglandin E1 (PGE1) (1 μg, 2 μl) injected intraventricularly did not alter plasma prolactin in ovariectomized, estrogentreated rats. When this dose of PGE1 was injected 5 min before the injection of other agents, it completely prevented the effect of DA and partially that of A, but failed to modify the decrease in plasma prolactin induced by DBC. Since these experiments were carried out in ether-anesthetized animals, additional experiments were performed in conscious rats in which blood samples were drawn through a permanent cannula implanted in the external jugular vein. Under these conditions, third ventricular injections of A (20 μg, 4 μl) or DBC (0.10M, 2 μl) again decreased plasma prolactin titers. Saline solution (4 μl) or 5′ AMP (0.10M, 2 μl) were ineffective. On the contrary, the intraventricular injection of morphine (20 μg, 4 μl) markedly increased plasma prolactin. None of the substances injected, except PGE1, modified plasma LH titers, PGE1 significantly increased LH levels 15 min after its 3rd V injection. These results suggest that the inhibitory effect that DA exerts on prolactin release through release of prolactin-inhibiting factor (PIF) may be mediated by an activation of the cyclic AMP system and inhibited by an increase in intracellular PGE1 concentration.
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