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Vol. 16, No. 3-4, 1974
Issue release date: 1974
Section title: Paper
Neuroendocrinology 1974;16:178–190
(DOI:10.1159/000122564)

Effect of Gamma-Aminobutyric Acid (GABA) and GABA Antagonist Drugs on ACTH Release

Makara G.B. · Stark E.
Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest

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Article / Publication Details

First-Page Preview
Abstract of Paper

Received: 12/5/1973
Accepted: 6/4/1974
Published online: 3/20/2008
Issue release date: 1974

Number of Print Pages: 13
Number of Figures: 0
Number of Tables: 0

ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)

For additional information: http://www.karger.com/NEN

Abstract

Corticotrophin (ACTH) release has been studied in rats given intraventricular gamma-aminobutyric acid (GABA) infusions or injections of picrotoxin and bicuculline. As an index of ACTH release the corticosterone level of blood or plasma was determined. GABA (1 M/liter), infused at a rate of 1 µl/min into the 3rd ventricle, inhibited the rise in plasma corticosterone normally produced by surgical trauma. 60 min after surgical trauma the rats given GABA infusions had lower blood corticosterone levels than the control rats given infusions of 1 M/liter of proline, 1 M/liter of glycine, or 0.15 M/liter of sodium chloride. Picrotoxin, an antagonist of GABA, is a potent stimulus of ACTH release. In sub-convulsive intraperitoneal doses it produced a significant rise in plasma corticosterone in conscious rats with complete hypothalamic deafferentation. Under pentobarbital anesthesia 12.5 µg of picrotoxin injected into the 3rd ventricle produced a small but significant rise in plasma corticosterone in rats with hypothalamic deafferentation. After intraventricular injections of bicuculline methiodide a significant rise in plasma corticosterone occurred in rats with hypothalamic deafferentation; the ACTH releasing effect of 2.5 µg of bicuculline methiodide was strongly inhibited by a simultaneous infusion of 0.15 M/liter of GABA. On the basis of this pharmacological evidence, we suggest that GABA may be an inhibitory neurotransmitter of hypothalamic interneurons and/or afferent pathways involved in the regulation of ACTH release.

© 1974 S. Karger AG, Basel


  

Author Contacts

Request reprints from: G.B. Makara, Institute of Experimental Medicine, Hungarian Academy of Sciences, P.O.B. 67, 1450 Budapest (Hungary)

  

Article Information

Received: December 5, 1973
Revised MS accepted: June 4, 1974
Published online: March 20, 2008
Number of Print Pages : 13

  

Publication Details

Neuroendocrinology (International Journal for Basic and Clinical Studies on Neuroendocrine Relationships)

Vol. 16, No. 3-4, Year 1974 (Cover Date: 1974)

Journal Editor: Millar R.P. (Edinburgh)
ISSN: 0028–3835 (Print), eISSN: 1423–0194 (Online)

For additional information: http://www.karger.com/NEN


Article / Publication Details

First-Page Preview
Abstract of Paper

Received: 12/5/1973
Accepted: 6/4/1974
Published online: 3/20/2008
Issue release date: 1974

Number of Print Pages: 13
Number of Figures: 0
Number of Tables: 0

ISSN: 0028-3835 (Print)
eISSN: 1423-0194 (Online)

For additional information: http://www.karger.com/NEN


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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