1991 Fiscal Year Final Research Report Summary
Synaptic plasticity in sex steroid-sensitive motoneurons.
| Project/Area Number |
01540621
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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., Assistance Prof., 医学部, 講師 (80053263)
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| Project Period (FY) |
1989 – 1991
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| Keywords | Gap junction / connexin 32 / mRNA / in situ hybridization / androgen / rat / lumbar spinal cord / motoneuron |
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| Research Abstract |
Gap junctions are considered to play an important role in metabolic and electrical coupling between neurons. We studied androgenic influence on the expression of the mRNA for gap junction protein in the androgen-sensitive motoneurons in the spinal nucleus of the bulbocavernosus(SNB)by using in situ hybridization histochemistry. A complementary DNA specific for the mRNA for r liver gap junction protein(connexin 32, a gift from Dr. D. A. Goodenough, Harvard Medical Sch was applied to in situ hybridization.
1. Cellular localization of gap junction mRNA was examined in the neonatal male rat brai Autoradiographic signals for connexin 32 mRNA were found to distribute in various regions of the brain such as parietal cortex, hippocampus, thalamus/striatum and hypothalamus. These signals were localized on neuronal cells. Immunohistochemical and ultrastructural observations of the hippocampus supported the presence of gap junctions in the examined region.
2. Cellular localization of gap junction m
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RNA was examined in the lumbar spinal cords of adult male rats. Autoradiographic-signals for connexin 32 mRNA were found to be localized on the somata and proximal dendrites of motoneurons in the SNB, dorsolateral nucleus(DLN)and retrodorsolateral nucleus(RDLN).
3. Adult male rats were castrated and implanted with Silastic tubes containing testosterone or nothing. Animals were sacrificed 4 weeks later. The removal of androgen by castration dramatically reduced the expression of gap junction mRNA in the androgen-sensitive SNB motoneurons, whereas this change was prevented by testosterone treatment. On the contrary, castration or testosterone treatment did not induce any changes in the expression level of gap junction mRNA in the androgen-insensitive RDLN motoneurons. These results suggest that androgen influences the expression of gap junction gene in the SNB motoneurons and may provide evidence for the molecular mechanisms of hormonally induced synaptic plasticity in the SNB motoneurons. Less
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