Thyrotropin-Releasing Hormone as a Mediator of the Central Autonomic Pathway Controlling Ovarian Function

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Abstract

We studied the effect of thyrotropin-releasing hormone (TRH) applied centrally on the sympathetic activity of the ovary in female rats. Intracerebroventricular (i.c.v.) administration of a dose of 25 ng/kg weight produced an increase in noradrenaline (NA) content at the ovary after 5 days of hormone administration. However, higher doses in a range up to 500 ng/kg weight decreased NA content at the ovary. At the celiac ganglia (where the cell bodies of sympathetic neurons projecting to the ovary originate) there was an accumulation of NA in spite of a decrease in tyrosine hydroxylase activity (T-OH). After cold exposure, opposite effects on T-OH activity and no effects on NA in ganglia and in ovary were obtained. Besides, i.v. injection of TRH only induced a decrease in ovarian NA. In contrast to the increase in T<sub>3</sub> plasma levels obtained after the cold-stress procedure, none of the i.c.v. doses of TRH used produced changes in T<sub>3</sub> plasma levels, strongly suggesting that the effect on sympathetic activity is mediated by a central effect of TRH acting as a putative activator of ovarian sympathetic nerves.

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Neurocircuitry of stress: central control of the hypothalamo-pituitary-adrenocortical axis.

James P Herman, William E. Cullinan (1997)

Integration of the hypothalamo-pituitary-adrenal stress response occurs by way of interactions between stress-sensitive brain circuitry and neuroendocrine neurons of the hypothalamic paraventricular nucleus (PVN). Stressors involving an immediate physiologic threat ('systemic' stressors) are relayed directly to the PVN, probably via brainstem catecholaminergic projections. By contrast, stressors requiring interpretation by higher brain structures ('processive' stressors) appear to be channeled through limbic forebrain circuits. Forebrain limbic sites connect with the PVN via interactions with GABA-containing neurons in the bed nucleus of the stria terminalis, preoptic area and hypothalamus. Thus, final elaboration of processive stress responses is likely to involve modulation of PVN GABAergic tone. The functional and neuroanatomical data obtained suggest that disease processes involving inappropriate stress control involve dysfunction of processive stress pathways.

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Stress and the adrenocortical control of epinephrine synthesis.

Richard J. Wurtman (2002)

Psychologic states produced by environmental or physiologic stresses are usually associated with hypersecretion of adrenal hormones, particularly epinephrine and the glucocorticoids (hydrocortisone in humans or corticosterone in rats). A common mechanism links the secretion of these hormones, even though the adrenal medulla and cortex have different embryologic origins and biochemical properties and very different mechanisms controlling their secretory activities, ie, a cholinergic nervous input stimulates medullary secretion while a hormone, corticotropin (ACTH), activates secretion from the cortex. This mechanism is made possible by an intra-adrenal portal vascular system, which provides the medulla with uniquely high concentrations of glucocorticoids. These high concentrations are needed to induce the medullary enzyme, phenylethanolamine-N-methyltransferase (PNMT), which controls the synthesis of epinephrine from norepinephrine. By suppressing glucocorticoid secretion, pituitary failure compromises epinephrine synthesis and decreases the rate at which epinephrine is secreted; in contrast, prolonged chronic stress can enhance epinephrine synthesis and secretion within the adrenal, the brain, or both organs. This control mechanism could be involved in the long-term consequences of stress.

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Sympathetic nervous system activation by glutamate injections into the paraventricular nucleus.

Douglas S. Martin, Joseph Haywood (1992)

The purpose of the present study was to determine the overall cardiovascular and sympathetic nervous system responses to stimulation of neuronal cell bodies in the paraventricular nucleus (PVN) of the hypothalamus. Bilateral microinjections (50 nl) of monosodium glutamate or sodium acetate were made into the PVN of conscious unrestrained rats. Blood pressure, heart rate and plasma concentrations of norepinephrine and epinephrine were measured. The injection of sodium acetate as an osmotic control was without effect on any of the recorded variables. In contrast, the injections of glutamate were associated with a rapid increase in both blood pressure and heart rate. At doses of 15, 25, and 50 nmol blood pressure increased by 13 +/- 2, 14 +/- 3 and 16 +/- 1 mmHg while heart rate increased by 64 +/- 15, 73 +/- 8 and 50 +/- 8 bpm. These responses were associated with increases in plasma norepinephrine concentrations of 51 +/- 8, 100 +/- 16 and 62 +/- 13 pg/ml while epinephrine concentrations rose by 42 +/- 17, 58 +/- 18 and 38 +/- 17 pg/ml. The responses of glutamate (25 nmol) were not affected by blockade of vascular vasopressin receptors with d(CH2)5Tyr(Me)AVP (10 micrograms/kg) (blood pressure: pre 15 +/- 3 vs post 13 +/- 3 mmHg, heart rate: pre 77 +/- 9 bpm vs post 91 +/- 7 bpm, plasma norepinephrine: pre 106 +/- 22 vs post 121 +/- 28 pg/ml and plasma epinephrine: pre 61 +/- 25 vs post 34 +/- 30 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

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Author and article information

Journal

Journal ID (publisher-id): NEN

Journal ID (nlm-ta): Neuroendocrinology

Journal ID (doi): 10.1159/issn.0028-3835

Title: Neuroendocrinology

Publisher: S. Karger AG

ISSN (Print): 0028-3835

ISSN (Electronic): 1423-0194

Publication date Subscription-year: 2003

Publication date (Print): April 2003

Publication date (Electronic): 21 May 2003

Volume: 77

Issue: 4

Pages: 273-281

Affiliations

^aLaboratory of Neurobiochemistry, Department of Biochemistry and Molecular Biology, Faculty of Chemistry and Pharmaceutical Sciences, Santiago, Chile; ^bLaboratory of Cerebral Plasticity, UMR 5102 from CNRS, University of Montpellier 2, Montpellier, France; ^cClinical Hospital, Universidad de Chile, Santiago, Chile

Article

Publisher ID: 70282 Other ID: Neuroendocrinology 2003;77:273–281

DOI: 10.1159/000070282

PubMed ID: 12766327

SO-VID: 48beb30f-0e68-4a64-8704-9d7468a2b804

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. 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 government 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. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 14 August 2002

Date accepted : 31 January 2003

Page count

Figures: 4, Tables: 2, References: 57, Pages: 9

Thyrotropin-Releasing Hormone as a Mediator of the Central Autonomic Pathway Controlling Ovarian Function

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Abstract

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Karger: Endocrinology

Most cited references 19

Neurocircuitry of stress: central control of the hypothalamo-pituitary-adrenocortical axis.

Stress and the adrenocortical control of epinephrine synthesis.

Sympathetic nervous system activation by glutamate injections into the paraventricular nucleus.

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