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dc.contributor.advisor Sengelaub, Dale R. en_US
dc.contributor.author Fargo, Keith Nolan en_US
dc.date.accessioned 2010-06-01T17:46:27Z
dc.date.available 2027-02-01T18:46:28Z
dc.date.available 2010-06-09T13:32:31Z
dc.date.issued 2010-06-01T17:46:27Z
dc.date.submitted 2006 en_US
dc.identifier.uri http://hdl.handle.net/2022/7243
dc.description Thesis (PhD) - Indiana University, Neuroscience, 2006 en_US
dc.description.abstract Motoneuron loss is a significant medical problem that can result from traumatic injury or from disease processes. I have recently demonstrated that the unilateral injection of a retrogradely transported conjugate of the toxin saporin into the bulbocavernosus and levator ani muscles kills the majority of ipsilateral motoneurons that project to the injected musculature. In addition, and more importantly for this thesis, the contralateral motoneurons are also affected. While they are not killed, they display a massive retraction of their dendrites, as well as a loss of cross-sectional area. Morphological changes in surviving motoneurons might therefore account for some of the functional deficits produced by motoneuron loss. Treatment with exogenous testosterone, however, completely prevents the regressive morphological changes that follow partial motoneuron depletion, suggesting that steroid treatment could prove to be an important factor in combating the deleterious effects of motoneuron loss. The protective effect of testosterone treatment on the morphology of surviving motoneurons in this neuromuscular system raises several intriguing questions. In this thesis I describe a series of experiments undertaken in an attempt to answer some of these questions. In particular, I have explored the effects of motoneuron depletion and testosterone treatment on ipsilateral motoneuron pools; examined the effectiveness of testosterone treatment on the electrophysiological functioning of surviving motoneurons following motoneuron depletion; examined the effects of testosterone treatment after using another method of killing motoneurons--one which does not involve introducing an exogenous toxin into the spinal cord; and tested whether the beneficial effects of testosterone treatment following motoneuron depletion can be accounted for by its conversion to its metabolite estradiol. The most important findings are that testosterone treatment is effective in restoring some electrophysiological effects produced in surviving motoneurons following partial motoneuron depletion, and that the beneficial effects of testosterone on the morphology of surviving motoneurons is as androgen effect, rather than an estrogen effect. en_US
dc.language.iso EN en_US
dc.publisher [Bloomington, Ind.] : Indiana University en_US
dc.subject penile reflexes en_US
dc.subject steroids en_US
dc.subject cell death en_US
dc.subject spinal cord injury en_US
dc.subject saporin en_US
dc.subject ventral root avulsion en_US
dc.subject.classification Biology, Neuroscience en_US
dc.subject.classification Psychology, Psychobiology en_US
dc.title Testosterone as a neuroprotective/neurotherapeutic agent following partial neuronal depletion en_US
dc.type Doctoral Dissertation en_US


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