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Dexamethasone-Induced Suppression of Vasopressin Gene Expression in the Bed Nucleus of the Stria Terminalis and Medial Amygdala Is Mediated by Changes in Testosterone

Dexamethasone-Induced Suppression of Vasopressin Gene Expression in the Bed Nucleus of the Stria... Vasopressin (VP) neurons in the bed nucleus of the stria terminalis (BNST) and medial amygdala (AME) are sensitive to changes in circulating levels of testosterone (T). To determine whether these cells are responsive to changes in glucocorticoid levels, in situ hybridization and quantitative autoradiography were used to measure VP mRNA in cells of the BNST and AME in rats that were adrenalectomized (ADX; 14 days) or ADX with dexamethasone (DEX) replacement. These treatments produced the predicted changes in VP gene expression in the medial parvocellular group of the paraventricular nucleus. The VP mRNA content within cells of the BNST or AME was unaffected by adrenalectomy. Treatment with DEX significantly decreased both the number and labeling intensity of VP cells in the BNST and AME. Measurement of plasma T in these animals showed that DEX treatment significantly lowered mean T levels compared with those in either sham-operated or ADX animals. Adrenalectomy alone did not significantly alter T levels. To determine whether DEX influenced VP gene expression via a glucocorticoid action or secondarily by a suppression of T, the above experiment was repeated with groups that were castrated and implanted with Silastic capsules containing T to maintain physiological levels of T. Administration of DEX again decreased both VP cell number and labeling intensity of cells in the BNST and AME in sham-implanted animals. However, VP gene expression was unaffected in those animals that received T capsules. Administration of corticosterone did not alter T levels or the number of cells in the BNST or AME. These results suggest that, in contrast to paraventricular nucleus neurons, adrenalectomy (14 days) is not a potent stimulus in altering VP activity in the BNST or AME. The DEX-induced decrease in VP gene expression is mediated by a secondary suppression of T levels. These results support the finding that gonadal steroids are essential in maintaining the biosynthetic integrity of VP neurons in the BNST and AME. This content is only available as a PDF. Author notes * This work was supported in part by the Research Service of the Department of Veterans Affairs and NIH Grant NS-20311. † Recipient of a NIH National Research Services Award (1-F32-NS-08609) from the NINDS. Current address: Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60201. Copyright © 1991 by The Endocrine Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Endocrinology Oxford University Press

Dexamethasone-Induced Suppression of Vasopressin Gene Expression in the Bed Nucleus of the Stria Terminalis and Medial Amygdala Is Mediated by Changes in Testosterone

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References (26)

Publisher
Oxford University Press
Copyright
Copyright © 1991 by The Endocrine Society
ISSN
0013-7227
eISSN
1945-7170
DOI
10.1210/endo-129-1-109
Publisher site
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Abstract

Vasopressin (VP) neurons in the bed nucleus of the stria terminalis (BNST) and medial amygdala (AME) are sensitive to changes in circulating levels of testosterone (T). To determine whether these cells are responsive to changes in glucocorticoid levels, in situ hybridization and quantitative autoradiography were used to measure VP mRNA in cells of the BNST and AME in rats that were adrenalectomized (ADX; 14 days) or ADX with dexamethasone (DEX) replacement. These treatments produced the predicted changes in VP gene expression in the medial parvocellular group of the paraventricular nucleus. The VP mRNA content within cells of the BNST or AME was unaffected by adrenalectomy. Treatment with DEX significantly decreased both the number and labeling intensity of VP cells in the BNST and AME. Measurement of plasma T in these animals showed that DEX treatment significantly lowered mean T levels compared with those in either sham-operated or ADX animals. Adrenalectomy alone did not significantly alter T levels. To determine whether DEX influenced VP gene expression via a glucocorticoid action or secondarily by a suppression of T, the above experiment was repeated with groups that were castrated and implanted with Silastic capsules containing T to maintain physiological levels of T. Administration of DEX again decreased both VP cell number and labeling intensity of cells in the BNST and AME in sham-implanted animals. However, VP gene expression was unaffected in those animals that received T capsules. Administration of corticosterone did not alter T levels or the number of cells in the BNST or AME. These results suggest that, in contrast to paraventricular nucleus neurons, adrenalectomy (14 days) is not a potent stimulus in altering VP activity in the BNST or AME. The DEX-induced decrease in VP gene expression is mediated by a secondary suppression of T levels. These results support the finding that gonadal steroids are essential in maintaining the biosynthetic integrity of VP neurons in the BNST and AME. This content is only available as a PDF. Author notes * This work was supported in part by the Research Service of the Department of Veterans Affairs and NIH Grant NS-20311. † Recipient of a NIH National Research Services Award (1-F32-NS-08609) from the NINDS. Current address: Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois 60201. Copyright © 1991 by The Endocrine Society

Journal

Endocrinology – Oxford University Press

Published: Jul 1, 1991

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