| Project/Area Number |
06640869
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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 |
生物形態・構造
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| Research Institution | Juntento University School of Medicine |
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Principal Investigator |
MATSUMOTO Akira Juntendo University School of Medicine, Assoc. Prof., 医学部, 助教授 (80053263)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | rat / lumbar spinal cord / motoneuron / synapse / gamma-aminobutyric acid / androgen / immunohistochemistry / アンドロゲン / ラット |
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| Research Abstract |
Motoneurons of the spinal nucleus of the bulbocavernosus (SNB) of male rats innervate the perineal striated muscles bulbocavernosus and levator 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 synaptic connections in androgen-sensitive SNB motoneurons. To clarify molecular mechanisms of androgen for synaptic plasticity, we examined androgenic regulation of the expression of several kinds of neurotransmitters or neuromodulators such as glutamic acid, gamma-aminobutyric acid (GABA), tyrosine hydroxylase, enkephalin and substance P in the axon terminals making synaptic contact with SNB motoneurons of adult male rats by immunohistochemical analysis. Tyrosine hydroxylase-, enkephalin- or substance P-immunoreactive axon terminals were found to make synaptic contact with SNB motoneurons of intact male rats although the incidence of these terminals was very low. In contrast, a number of GABA-immunoreactive axon terminals making synaptic contact with SNB motoneurons were detected. Removal of androgen by castration significantly reduced the number of GABA-immunoreactive axon terminals, whereas the change was prevented by testosterone treatment. These results suggest that androgen regulates the incidence of GABA-immunoreactive axon terminals that synapse onto SNB motoneurons and may provide evidence for the molecular mechanisms of hormonally-induced synaptic plasticity in the SNB motoneuron.
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