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Endocrinology, doi:10.1210/endo-116-4-1327
Endocrinology Vol. 116, No. 4 1327-1333
Copyright © 1985 by the Endocrine Society.
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Electrophysiological Manifestation of Luteinizing Hormone-Releasing Hormone Pulse Generator Activity in the Rhesus Monkey: Influence of {alpha}-Adrenergic and Dopaminergic Blocking Agents*

JEAN-MARC KAUFMAN{dagger}, JAMES S. KESNER, RICHARD C. WILSON and ERNST KNOBIL

Departments of Physiology and Cell Biology and Neurobiology and Anatomy and the Laboratory for Neuroendocrinology, The University of Texas Medical School at Houston Houston, Texas 77225

Address requests for reprints to: Dr. Ernst Knobil, Laboratory for Neuroendocrinology, University of Texas Medical School at Houston, 7128 Medical School Building, P.O. Box 20708, Houston, Texas 77225.

Abstract

Characteristic increases in neuronal electrical activity associated with the initiation of each LH pulse were recorded from ovariectomized rhesus monkeys bearing multiple chronic electrodes in the medial basal hypothalamus. These electrophysiological manifestations of hypothalamic LHRH pulse generator activity were inhibited by the {alpha}-adrenergic blocker phentolamine or the {alpha}-adrenoceptor blockers phenoxybenzamine and prazosin. At the dosages used, the effects of single injections of these drugs ranged from a reduction in the frequency of LHRH pulse generator activity to its complete arrest. This was faithfully reflected in the pattern of pulsatile LH discharges. The dopaminergic blocking agent metaclopramide similarly reduced the frequency of the pulse generator or arrested its activity altogether. The {alpha}2-adrenoceptor blocker yohimbine had no demonstrable effect on hypothalamic electrical activity at the doses studied. These findings support the view of a central action of {alpha}-adrenergic and dopaminergic blockade on LHRH pulse generator activity and the concept that central adrenergic and dopaminergic inputs can modulate the frequency of the LHRH pulse generator. (Endocrinology 116: 1327-1333, 1985)

Footnotes

* This work was supported in part by Grants HD-17438 and HD-08610 from the NIH and a grant from the A. W. Mellon Foundation. preliminary report of this work was presented at the Seventh International Congress of Endocrinology, Quebec City, Canada, 1984 (Abstract 1232).

{dagger} Present address: Department of Endocrinology, Akademisch Ziekenhuis, DE Pintelaan 185, B9000 Ghent, Belgium.

Received August 17, 1984.




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