| Project/Area Number |
04640692
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
動物形態・分類学
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| Research Institution | Juntendo University School of Medicine |
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Principal Investigator |
MATSUMOTO Akira Juntendo Univ., Sch. Med., Assoc. Prof., 医学部, 助教授 (80053263)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1992: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | beta-actin / beta-tubulin / mRNA / in situ hydridization / androgen / rat / lumber spinal cord / motoneuron / beta-アクチン / beta-チューブリン |
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| Research Abstract |
Motoneurons of the spinal nucleus of the bulbocavornosus (SNB) of male rats innervate the perineal striated muscles bulbocavernosus and lavator ani that attach to the penis. They have an important role in copulatory behavior, which is sensitive to alterations in circulating levels of androgen. Androgen is also known to play a crucial role in reorganizing the neuronal elements and synaptic connections in androgen-sensitive SNB motoneurons. To clarify molecular mechanisms of androgen for neuronal plasticity, we examined androgenic regulation of the mRNA expression of cytoskeletal proteins such as beta-actin and beta-tubulin in the SNB motoneurons of adult male rats. Adult male rats were castrated and implanted with silastic tubes containing testosterone or nothing. Animals were sacrificed 4 weeks later. Chick beta-actine and mouse beta-tubulin complementary CNAs were used to detect mRNAs encoding beta-actin and beta-tubulin of the SNB motoneurons, respectively. The radiolabeled DNA probes were applied o in situ hybridization histochemistry. Motoneurons in the retrodorsolateral nucleus (RDLN), which innervate hindlimb musculature, were also examined. Autoradiographic signals for beta-actin and beta-tubulin mRNAs were found to be localized on the somata and proximal dendrites of SNB and RDLN motoneurons. Removal of androgen by castration significantly reduced the expression level of these mRNAs in the SNB motoneurons, whereas the change was prevented by testosterone treatment. ON the contrary, castration or testosterone treatment did not induce any changes in the expression level of these mRNAS in androgen-insensitive RDLN motoneurons. These results suggest that androgen regulates the expression of cytoskeletal protein genes in the SNB motoneurons and may provide evidence for the molecular mechanisms of hormonally-induced neuronal plasticity in the SNB motoneuron.
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