This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by JOHNSTON, C. A. Articles by NEGRO-VILAR, A. Search for Related Content PubMed PubMed Citation Articles by JOHNSTON, C. A. Articles by NEGRO-VILAR, A.

Prolactin Release after 5-Hydroxytryptophan Treatment Requires an Intact Neurointermediate Pituitary Lobe^*

CRAIG A. JOHNSTON, KATHERINE D. FAGIN, RICHARD H. ALPER and ANDRÈS NEGRO-VILAR

Reproductive Neuroendocrinology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health Research Triangle Park, North Carolina 27709;
The Department of Physiology, University of California San Francisco, California 94143

Address requests for reprints to: Dr. Andres Negro-Vilar, Reproductive Neuroendocrinology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, P.O. Box 12233, Research Triangle Park, North Carolina 27709.

Abstract

The present study was designed to evaluate the role of the neurointermediate pituitary lobe (NIL) in the 5-hydroxytryptophan (5-HTP)-induced increase in plasma PRL levels. The neurochemical mechanisms involved in this neuroendocrine regulation were also analyzed by examining the concentrations of serotonin (5-HT), norepinephrine, and dopamine as well as their primary metabolites in the median eminence (ME), NIL, and anterior pituitary (AP) after different treatments. Removal of the NIL (NIL-X) did not significantly affect basal plasma PRL concentrations or amine metabolism in the ME or AP. 5-HTP administration resulted in a 5-fold increase in plasma PRL in sham-operated (SHAM) animals, but NIL-X completely abolished this PRL response. 5-HTP injection elicited large increases in 5-HT and 5-hydroxyindole-3-acetic acid concentrations in ME, NIL, and AP in SHAM animals, and similar changes within the ME and AP in NIL-X animals, but did not significantly affect norepinephrine or dopamine metabolism in the ME, NIL, or AP of NIL-X or SHAM animals. Moreover, tissue concentrations of 5-HTP after 5-HTP injection increased similarly in SHAM and NIL-X animals. Inhibition of peripheral decarboxylase activity with MK486 prevented the 5- HTP-induced increase in PRL in SHAM animals and the increase in 5-HT metabolism in both SHAM and NIL-X groups. These data indicate that an intact NIL is required for the 5- HTP-induced increase in plasma PRL, but does not seem to be essential for the regulation of basal PRL release. They also demonstrate that the 5-HTP-induced activation of 5-HT metabolism in both ME and AP is not sufficient, by itself, to enhance PRL release. (Endocrinology 118: 805-810,1986)

Footnotes

^* Animals and Surgical and animal facilities were paid for by NIH Grant AM-28172 (to Dr. Mary F. Dallman, U.C.S.F.).

Supported by NIH Grant AM-07265.

Received March 8, 1985.

This article has been cited by other articles:

				A. Papageorgiou and C. Denef Estradiol Induces Expression of 5-Hydroxytryptamine (5-HT) 4, 5-HT5, and 5-HT6 Receptor Messenger Ribonucleic Acid in Rat Anterior Pituitary Cell Aggregates and Allows Prolactin Release via the 5-HT4 Receptor Endocrinology, March 1, 2007; 148(3): 1384 - 1395. [Abstract] [Full Text] [PDF]