A Testicular Influence on Restraint-Induced Activation of Medial Parvocellular Neurons in the Paraventricular Nucleus in the Male Rat
Author(s) -
Victor Viau,
Patricia Lee,
Jeff Sampson,
Janice Wu
Publication year - 2003
Publication title -
endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.674
H-Index - 257
eISSN - 1945-7170
pISSN - 0013-7227
DOI - 10.1210/en.2003-0064
Subject(s) - parvocellular cell , medicine , endocrinology , vasopressin , corticosterone , nucleus , testosterone (patch) , chemistry , hypothalamus , biology , hormone , neuroscience
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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