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Electrophysiological Studies on Cerebellar Synaptic Transmission in P/Q-type Ca2+ Channel Mutant Mice
https://ir.soken.ac.jp/records/1117
https://ir.soken.ac.jp/records/1117c9efd12e-420c-41ac-8a8d-05789eeb5b77
| 名前 / ファイル | ライセンス | アクション |
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要旨・審査要旨 / Abstract, Screening Result (189.8 kB)
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本文 (1.5 MB)
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| Item type | 学位論文 / Thesis or Dissertation(1) | |||||
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| 公開日 | 2010-02-22 | |||||
| タイトル | ||||||
| タイトル | Electrophysiological Studies on Cerebellar Synaptic Transmission in P/Q-type Ca2+ Channel Mutant Mice | |||||
| タイトル | ||||||
| タイトル | Electrophysiological Studies on Cerebellar Synaptic Transmission in P/Q-type Ca2+ Channel Mutant Mice | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_46ec | |||||
| 資源タイプ | thesis | |||||
| 著者名 |
松下, かおり
× 松下, かおり |
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| フリガナ |
マツシタ, カオリ
× マツシタ, カオリ |
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| 著者 |
MATSUSHITA, Kaori
× MATSUSHITA, Kaori |
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| 学位授与機関 | ||||||
| 学位授与機関名 | 総合研究大学院大学 | |||||
| 学位名 | ||||||
| 学位名 | 博士（理学） | |||||
| 学位記番号 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 総研大甲第561号 | |||||
| 研究科 | ||||||
| 値 | 生命科学研究科 | |||||
| 専攻 | ||||||
| 値 | 20 生理科学専攻 | |||||
| 学位授与年月日 | ||||||
| 学位授与年月日 | 2001-09-28 | |||||
| 学位授与年度 | ||||||
| 値 | 2001 | |||||
| 要旨 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Recent genetic and molecular biological analyses have revealed many forms of inherited channelopathies, and single gene mutations is directly responsible for the neurological phenotypes. Homozygous ataxic mice, tottering (tg) and rolling Nagoya (tg<SUP>rol</SUP>), have mutations in the P/Q-type Ca<SUP>2+</SUP> channel α<SUB>1A</SUB> subunit gene. The location of the mutations and the neurological phenotypes are known, but the mechanisms how the mutations cause the symptoms and how the different mutations lead to various onset and severity have remained unsolved. Here she compared fundamental properties of excitatory synaptic transmission in the cerebellum and its sensitivity to subtype-specific Ca<SUP>2+</SUP> channel blockers among wild-type control, tg, and tg<SUP>rol</SUP> mice. The amplitude of excitatory posysynaptic current (EPSC) of the parallel fiber-Purkinje cell (PF-PC) synapses was considerably reduced in ataxic tg<SUP>rol</SUP>. Whereas the PF-PC EPSC was only mildly decreased in non-alaxic tg mice, the PF-PC EPSC was drastically diminished in ataxic tg mice of P28-35. In contrast, the EPSC amplitude of the climbing fiber-Purkinje cell (CF-PC) synapses was preserved in tg, and it was even increased in tg<SUP>rol</SUP>. CF-PC EPSC was more dependent on the N- and R-types in mutant mice, suggesting that such compensatory mechanisms maintain the CF-PC synaptic transmission virtually intact. The results indicate that the impairment of the PF-PC synaptic transmission well correlates with manifestation of ataxia, and that different mutations of the P/Q- type Ca<SUP>2+</SUP> channel not only cause the primary effect of various severity but also lead to diverse secondary effects, which include up-regulation of other Ca<SUP>2+</SUP> channel subtypes and enhancement of sensitivity of postsynaptic glutamate receptors. | |||||
| 所蔵 | ||||||
| 値 | 有 | |||||
