Functional roles of leak K+ channels in injured motoneurons

泄漏 K 通道在受损运动神经元中的功能作用

• 批准号: 21700432
• 负责人: TOYODA Hiroki
• 金额: $ 2.83万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21700432/
• 关键词: 漏洩K^+チャネル; ニューロン; 一酸化窒素; 漏洩カリウムチャネル; 神経損傷; 神経麻痺; リークカリウムチャネル

It is known that production of nitric oxide (NO) is enhanced in injured motoneurons after peripheral nerve injury, The enhanced NO production is thought to contribute to the occurrence of nerve paralysis, However, it remains unknown how the enhanced NO production induces nerve paralysis, In this study, I focused on the changes in the membrane excitability by NO as the mechanism of neural paralysis, In particular, I studied on the NO-mediated modulation of leak K^+ currents, which regulate the resting membrane potential and the input resistance, Following application of 8-Br-cGMP, leak K^+ currents were decreased in large-sized motoneurons, while those were increased in small-sized motoneurons, These results suggest that activation of NO-cGMP-PKG pathway alters the membrane excitability of motoneurons through modulating the leak K^+ currents, It is possible that such neural mechanisms are involved in the occurrence of neural paralysis,

众所周知，周围神经损伤后受伤的运动神经元的一氧化氮（NO）的产生增强了，认为没有产生没有产生会导致神经瘫痪的发生，但是，未知的没有增强的产生如何诱导神经瘫痪，，神经瘫痪，，神经瘫痪是如何的在这项研究中，我专注于膜兴奋性的变化，尤其是神经瘫痪的机制，我研究了NO介导的泄漏K^+电流的调节，这些调节调节了静息膜电位和输入电阻，在应用8-BR-CGMP后，大型运动神经元中泄漏K^+电流降低，而小型运动神经元中这些电流的增加，这些结果表明，NO-CGMP-PKG途径的激活改变了膜的兴奋性通过调节泄漏K+电流的运动神经元，这种神经机制可能参与神经瘫痪的发生，

项目成果

Rank-ordered recruitment of masseter motoneurons by the activity of mesencephalic trigeminal neurons during slow closing phase of mastication cycle

在咀嚼周期缓慢结束阶段，中脑三叉神经元的活动对咬肌运动神经元的有序募集

• 发表时间: 2010
• 期刊: Journal of Oral Bioscience.
• 作者: Kang Y;Saito M;Toyoda H;Sato H
• 通讯作者: Sato H

Enhanced synaptic long-term potentiation in the interior cingulate cortex of adult wild mice as compared with that in laboratory mice.

与实验室小鼠相比，成年野生小鼠内部扣带皮层的突触长期增强增强。

• 发表时间: 2009
• 期刊: Molecular Brain 11
• 作者: Zhao;M.G.;et al.
• 通讯作者: et al.

咬筋運動ニューロンにおけるTASKチャネルの発現様式

咬肌运动神经元TASK通道的表达模式

• 发表时间: 2009
• 作者: 平尾圭子;豊田博紀;齋藤充;佐藤元;姜英男
• 通讯作者: 姜英男

咬筋運動ニューロンにおける漏痩K(+)電流に対するPKGの調節作用

PKG对咬肌运动神经元失活K(+)电流的调节作用

• 发表时间: 2009
• 作者: 豊田博紀;他
• 通讯作者: 他

Protein kinase G (PKG) bidirectionally modulates TASK1 currents in PKG-loaded HEK 293 cells.

蛋白激酶 G (PKG) 双向调节 PKG 负载的 HEK 293 细胞中的 TASK1 电流。

• 发表时间: 2010
• 作者: Toyoda H;Saito M;Okazawa M;Hirao K;Sato H;Abe H;Takada K;Funabiki K;Takada M;Kaneko T;Kang Y.
• 通讯作者: Kang Y.