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  1. 020 学位論文
  2. 生命科学研究科
  3. 20 生理科学専攻

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/1117
c9efd12e-420c-41ac-8a8d-05789eeb5b77
名前 / ファイル ライセンス アクション
甲561_要旨.pdf 要旨・審査要旨 / Abstract, Screening Result (189.8 kB)
甲561_本文.pdf 本文 (1.5 MB)
Item type 学位論文 / Thesis or Dissertation(1)
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
言語 en
タイトル Electrophysiological Studies on Cerebellar Synaptic Transmission in P/Q-type Ca2+ Channel Mutant Mice
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

WEKO 9369

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

WEKO 9370

マツシタ, カオリ

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著者 MATSUSHITA, Kaori

× MATSUSHITA, Kaori

WEKO 9371

en 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
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.
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