Possible role of cyclic AMP and prostaglandin E1 in the dopaminergic control of prolactin release

Sergio Ojeda, P. G. Harms, S. M. McCann

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

In ovariectomized, estrogen treated rats (10 μg estradiol benzoate, luteinizing hormone, 48 hr before) bearing a permanent cannula in the third ventricle (3rd V), the third ventricular injection of dopamine (DA) (2 μg), but not norepinephrine (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 decreased in 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 s.c. 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, estrogen treated 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 luteinizing hormone (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 inactivation of the cyclic AMP system and inhibited by an increase in intracellular PGE1 concentration.

Original languageEnglish (US)
Pages (from-to)1694-1703
Number of pages10
JournalEndocrinology
Volume95
Issue number6
StatePublished - 1974
Externally publishedYes

Fingerprint

Alprostadil
Prolactin
Cyclic AMP
Bucladesine
Dopamine
Luteinizing Hormone
Injections
Adenosine Monophosphate
Sodium Chloride
Prolactin Release-Inhibiting Factors
Estrogens
Intraventricular Injections
Pimozide
Third Ventricle
Apomorphine
Jugular Veins
Ether
Morphine
Norepinephrine

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Possible role of cyclic AMP and prostaglandin E1 in the dopaminergic control of prolactin release. / Ojeda, Sergio; Harms, P. G.; McCann, S. M.

In: Endocrinology, Vol. 95, No. 6, 1974, p. 1694-1703.

Research output: Contribution to journalArticle

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