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      On the Relationship between Noradrenergic Stimulatory and GABAergic Inhibitory Systems in the Control of Luteinizing Hormone Secretion in Female Rats

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          Abstract

          The relationship between noradrenergic (NA) stimulatory and γ-aminobutyric acid (GABA)-mediated inhibitory systems in the control of luteinizing hormone (LH) secretion was examined in ovariectomized rats. Stimulation of the GABAA receptor by an intraventricular (i.c.v.) administration of a GABAA agonist, muscimol, significantly attenuated the LH secretory response to the subsequent i.c.v. injection of NA in estrogen-primed rats. On the other hand, blockade of α-adrenergic receptors by phenoxybenzamine did not interfere with the stimulatory effect of an i.c.v. injection of a GABAA antagonist bicuculline. In a different series of experiments, ovariectomized animals had been treated with i.c.v. injections of 6-hydroxydopamine (6-OHDA) or its vehicle. An i.c.v. injection of muscimol or phentolamine significantly inhibited the estrogen-induced surge of LH secretion in vehicle-treated rats. Muscimol also inhibited the existing pulsatile LH secretion in vehicle-treated, estrogen-unprimed animals. In animals in which hypothalamic NA terminals were presumed to be destroyed by 6-OHDA, the inhibitory effect of phentolamine was significantly diminished while that of muscimol was unaltered. These results permit the following conclusions: (1) the central GABAergic system inhibits LH secretion via GABAA receptors; (2) this inhibitory GAB A system operates without mediation by the NA system, and (3) the GABAergic non-NA-mediated system can affect physiological patterns of pituitary LH secretion in female rats.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1990
          1990
          03 April 2008
          : 52
          : 6
          : 566-572
          Affiliations
          aDepartment of Physiology, St. Marianna University School of Medicine, Kawasaki; bDepartment of Physiology, Yokohama City, University School of Medicine, Yokohama, Japan
          Article
          125645 Neuroendocrinology 1990;52:566–572
          10.1159/000125645
          2178232
          © 1990 S. Karger AG, Basel

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          Page count
          Pages: 7
          Categories
          Original Paper

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