Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 7-Day Trial for You or Your Team.

Learn More →

Possible Role of Cyclic AMP and Prostaglandin E1 in the Dopaminergic Control of Prolactin Release

Possible Role of Cyclic AMP and Prostaglandin E1 in the Dopaminergic Control of Prolactin Release 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. (Endocrinology95: 1694, 1974) This content is only available as a PDF. Author notes 1 Present address: Physiology of Reproduction Section, Animal Science Department, Texas A&M University,College Station, Texas 77843. 2 Supported by grants from the Ford Foundation, NIH (AM 10073 and HD 01515) and the Texas Population Research Institute. Copyright © 1974 by The Endocrine Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Endocrinology Oxford University Press

Possible Role of Cyclic AMP and Prostaglandin E1 in the Dopaminergic Control of Prolactin Release

OJEDA, S., R.; HARMS, P., G.; MCCANN, S., M.
Endocrinology , Volume 95 (6) – Dec 1, 1974
Download PDF
10 pages

Loading next page...
 
/lp/oxford-university-press/possible-role-of-cyclic-amp-and-prostaglandin-e1-in-the-dopaminergic-2No0fY0zlN

References (0)

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

Publisher
Oxford University Press
Copyright
Copyright © 1974 by The Endocrine Society
ISSN
0013-7227
eISSN
1945-7170
DOI
10.1210/endo-95-6-1694
Publisher site
See Article on Publisher Site

Abstract

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. (Endocrinology95: 1694, 1974) This content is only available as a PDF. Author notes 1 Present address: Physiology of Reproduction Section, Animal Science Department, Texas A&M University,College Station, Texas 77843. 2 Supported by grants from the Ford Foundation, NIH (AM 10073 and HD 01515) and the Texas Population Research Institute. Copyright © 1974 by The Endocrine Society

Journal

Endocrinology – Oxford University Press

Published: Dec 1, 1974

There are no references for this article.