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Acute stimulation of prolactin release by estradiol: mediation by the posterior pituitary.
Endocrinology. 1990 Jun; 126(6):3179-84.E

Abstract

We have previously shown that the posterior pituitary contains a potent PRL-releasing factor (PRF). Estradiol stimulates PRL release by acting at three possible sites: the hypothalamus, the anterior pituitary, and the posterior pituitary. The objectives were 1) to document the profiles of PRL and LH release in response to an acute administration of estradiol, and 2) to identify the site of action of estradiol by employing two surgical approaches, pituitary stalk section (SS) and posterior pituitary lobectomy (LOBEX). Ovariectomized rats were used throughout. In Exp 1, rats were injected iv with 5 micrograms/kg 17 beta-estradiol, and blood was collected at 30-min intervals for 4 h. Estradiol induced a rapid and profound decline in plasma LH levels and a delayed, 5- to 6-fold rise in PRL. The purpose of the second experiment was to determine whether estradiol stimulates PRL release by acting at the anterior pituitary. Injection of estradiol to SS rats failed to stimulate a rise in PRL. We have previously reported that lactotrophs of SS rats are responsive to PRL secretagogues such as TRH. The objective of the third experiment was to differentiate between hypothalamic and posterior pituitary sites of estradiol action. Estradiol induced only a small rise in PRL when injected into LOBEX rats. However, LOBEX and control rats showed similar large rises in PRL in response to injection of alpha-methyl-para-tyrosine, an inhibitor of tyrosine hydroxylase. The latter indicates that the hypothalamic dopaminergic system as well as anterior pituitary lactotrophs are functionally intact in LOBEX rats. We conclude that estradiol administration to ovariectomized rats induces a rapid decline in LH and a delayed marked increase in PRL. The posterior pituitary, probably via PRF, is the primary site that mediates the acute effects of estradiol on PRL release. Estradiol does not stimulate PRL release directly from the anterior pituitary. The role of the hypothalamus is unclear. Estradiol could act directly on PRF-containing cells in the posterior pituitary or indirectly, via hypothalamic neurons terminating in the posterior pituitary. The hypothalamus also has a minor component that responds to estradiol and is independent of the posterior pituitary.

Authors+Show Affiliations

Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46223.No affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

2351112

Citation

Murai, I, and N Ben-Jonathan. "Acute Stimulation of Prolactin Release By Estradiol: Mediation By the Posterior Pituitary." Endocrinology, vol. 126, no. 6, 1990, pp. 3179-84.
Murai I, Ben-Jonathan N. Acute stimulation of prolactin release by estradiol: mediation by the posterior pituitary. Endocrinology. 1990;126(6):3179-84.
Murai, I., & Ben-Jonathan, N. (1990). Acute stimulation of prolactin release by estradiol: mediation by the posterior pituitary. Endocrinology, 126(6), 3179-84.
Murai I, Ben-Jonathan N. Acute Stimulation of Prolactin Release By Estradiol: Mediation By the Posterior Pituitary. Endocrinology. 1990;126(6):3179-84. PubMed PMID: 2351112.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acute stimulation of prolactin release by estradiol: mediation by the posterior pituitary. AU - Murai,I, AU - Ben-Jonathan,N, PY - 1990/6/1/pubmed PY - 1990/6/1/medline PY - 1990/6/1/entrez SP - 3179 EP - 84 JF - Endocrinology JO - Endocrinology VL - 126 IS - 6 N2 - We have previously shown that the posterior pituitary contains a potent PRL-releasing factor (PRF). Estradiol stimulates PRL release by acting at three possible sites: the hypothalamus, the anterior pituitary, and the posterior pituitary. The objectives were 1) to document the profiles of PRL and LH release in response to an acute administration of estradiol, and 2) to identify the site of action of estradiol by employing two surgical approaches, pituitary stalk section (SS) and posterior pituitary lobectomy (LOBEX). Ovariectomized rats were used throughout. In Exp 1, rats were injected iv with 5 micrograms/kg 17 beta-estradiol, and blood was collected at 30-min intervals for 4 h. Estradiol induced a rapid and profound decline in plasma LH levels and a delayed, 5- to 6-fold rise in PRL. The purpose of the second experiment was to determine whether estradiol stimulates PRL release by acting at the anterior pituitary. Injection of estradiol to SS rats failed to stimulate a rise in PRL. We have previously reported that lactotrophs of SS rats are responsive to PRL secretagogues such as TRH. The objective of the third experiment was to differentiate between hypothalamic and posterior pituitary sites of estradiol action. Estradiol induced only a small rise in PRL when injected into LOBEX rats. However, LOBEX and control rats showed similar large rises in PRL in response to injection of alpha-methyl-para-tyrosine, an inhibitor of tyrosine hydroxylase. The latter indicates that the hypothalamic dopaminergic system as well as anterior pituitary lactotrophs are functionally intact in LOBEX rats. We conclude that estradiol administration to ovariectomized rats induces a rapid decline in LH and a delayed marked increase in PRL. The posterior pituitary, probably via PRF, is the primary site that mediates the acute effects of estradiol on PRL release. Estradiol does not stimulate PRL release directly from the anterior pituitary. The role of the hypothalamus is unclear. Estradiol could act directly on PRF-containing cells in the posterior pituitary or indirectly, via hypothalamic neurons terminating in the posterior pituitary. The hypothalamus also has a minor component that responds to estradiol and is independent of the posterior pituitary. SN - 0013-7227 UR - https://www.unboundmedicine.com/medline/citation/2351112/Acute_stimulation_of_prolactin_release_by_estradiol:_mediation_by_the_posterior_pituitary_ L2 - https://academic.oup.com/endo/article-lookup/doi/10.1210/endo-126-6-3179 DB - PRIME DP - Unbound Medicine ER -