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Endocrinology, doi:10.1210/en.2003-0064
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*Compound via MeSH
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*TESTOSTERONE
Endocrinology Vol. 144, No. 7 3067-3075
Copyright © 2003 by The Endocrine Society

A Testicular Influence on Restraint-Induced Activation of Medial Parvocellular Neurons in the Paraventricular Nucleus in the Male Rat

Victor Viau, Patricia Lee, Jeff Sampson and Janice Wu

Department of Anatomy and Cell Biology, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3

Address all correspondence and requests for reprints to: Dr. Victor Viau, Department of Anatomy and Cell Biology, University of British Columbia, 2177 Wesbrook Mall, Vancouver, British Columbia, Canada V6T 1Z3. E-mail: viau{at}interchange.ubc.ca.

To gauge the strength by which the testes influence stress-induced activation of neurosecretory neurons in the paraventricular nucleus, we studied within medial parvocellular neurons the effects of gonadectomy on restraint-induced Fos-immunoreactivity and on CRH and arginine vasopressin (AVP) heteronuclear (hn) RNA expression levels. Relative to intact male rats (sham-gonadectomized), gonadectomized rats showed a significantly greater number of medial parvocellular neurons recruited to express Fos protein evident at 0.5 h and from 1–4 h after the onset of 30-min restraint exposure. Restraint provoked a transient increase in hnCRH levels that was maximal at the end of restraint and this was significant only in gonadectomized rats. Both intact and gonadectomized rats displayed an increase in AVP hnRNA expression levels in response to restraint exposure; however, it was significantly greater in gonadectomized rats. All of these responses were accompanied by a higher corticosterone response in gonadectomized compared with intact rats and negatively correlated with plasma testosterone concentrations, with the exception of stress-induced CRH transcription. These findings indicate an inhibitory role for testosterone on stress-induced indexes of synaptic (Fos) and transcriptional (AVP hnRNA) activation among hypophysiotropic paraventricular neurons and provide meaningful end points with which to pursue how and where androgens operate on stress-related input to the paraventricular nucleus motor neurons.




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