Literature DB >> 11164770

Testosterone modulates the dendritic architecture of arcuate neuroendocrine neurons in adult male rats.

S C Danzer1, N T McMullen, N E Rance.   

Abstract

Recent studies have demonstrated that gonadectomy of adult male rats induces dendritic growth of neuroendocrine neurons in the arcuate nucleus. We have hypothesized that these changes are secondary to the loss of testosterone negative feedback. In the present study, we examined the effects of testosterone replacement on the dendritic morphology of arcuate neuroendocrine neurons in castrated rats. Rats were orchidectomized and implanted with silastic capsules designed to produce physiological levels of plasma testosterone (n=9) or empty silastic capsules (n=9) for 2 months. Retrograde labeling with systemically injected Fluoro-Gold, followed by intracellular injection of labeled neurons in a fixed slice preparation, were used to visualize arcuate neuroendocrine neurons. Quantitative analysis of dendritic morphology was performed using three-dimensional computer reconstruction. Serum levels of LH (luteinizing hormone) and testosterone were measured by radioimmunoassay. Treatment of castrated rats with physiological levels of testosterone significantly reduced dendritic length, volume and terminal branch number relative to the castrated rats receiving empty silastic capsules. Dendritic spine density was also greater in the testosterone-treated animals, although the total numbers of spines per dendrite was not significantly different between the two groups. In addition, testosterone replacement was effective in reducing serum LH to levels found in intact rats. These studies demonstrate that testosterone replacement suppresses the dendritic outgrowth of arcuate neuroendocrine neurons that occurs in response to castration. The parallel changes in dendritic arbor and serum LH after castration and hormone replacement suggests that the suppressive effects of testosterone are related to steroid negative feedback.

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Year:  2001        PMID: 11164770     DOI: 10.1016/s0006-8993(00)03083-3

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


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