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Role of testosterone in the regulation of tuberoinfundibular dopaminergic neurons in the male rat
Authors:T W Toney  K J Lookingland  K E Moore
Affiliation:Department of Pharmacology and Toxicology, Michigan State University, East Lansing.
Abstract:The effects of testosterone on the tuberoinfundibular dopamine (DA) neuronal activity was examined by determining the rate of DA synthesis-accumulation of 3,4-dihydroxyphenylalanine (DOPA) after administration of a decarboxylase inhibitor and the concentration of a DA metabolite,--3,4-dihydroxyphenylacetic acid (DOPAC)--in the median eminence in the male rat. Within 1 week after orchidectomy, there was an increase in the accumulation of DOPA and the concentration of DOPAC in the median eminence, but there was no change in the concentration of DA. Conversely, 1 day after testosterone administration to orchidectomized rats, the elevated DOPAC concentrations in the median eminence returned to levels comparable to those in gonadally intact rats. Neither orchidectomy nor testosterone replacement had any effect on plasma prolactin concentrations, but inhibition of prolactin secretion following administration of the DA agonist bromocriptine blocked the increase in DOPA accumulation in the median eminence of orchidectomized rats; this latter effect was reversed by intracerebroventricular administration of prolactin. On the other hand, intracerebroventricular injection of prolactin caused a similar increase in the accumulation of DOPA in the median eminence of gonadally intact, orchidectomized, and testosterone-treated orchidectomized rats. Immobilization stress decreased the accumulation of DOPA and the concentration of DOPAC in the median eminence of orchidectomized rats, but had no effect in intact or testosterone-treated orchidectomized rats. These results indicate that testosterone inhibits the basal activity of tuberoinfundibular DA neurons and blocks the inhibitory effects of physical restraint on these neurons, but does not alter the ability of these neurons to respond to delayed activation by prolactin.
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