The elucidation of molecular basis on mechanisms for chemosensitive respiratory regulation

化学敏感性呼吸调节机制的分子基础阐明

• 批准号: 21790231
• 负责人: HIRATA Yutaka
• 金额: $ 2.75万
• 依托单位: Hyogo College of Medicine
• 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-21790231/
• 关键词: TRP; 中枢化学受容器; グリア細胞; カルシウム応答; 二酸化炭素; 水素イオン濃度; 延髄; 培養細胞

The medulla contains central chemosensitive cells (CRC) important for the maintenance of blood gas and pH homeostasis. To identify the intrinsic CRC, we measured responses of intracellular Ca^<2+> and H^+, and membrane potential of rat primary-cultured medullary cells to a brief exposure (sec level) to hypercapnic acidosis. In glia-rich cultures, intracellular acidification preceded the hypercapnic acidosis-induced Ca^<2+> response independent of extracellular pH. TRP channel blockers attenuated the hypercapnic acidosis-induced Ca^<2+> response. Subpopulations of cells that exhibited the hypercapnic acidosis-induced Ca^<2+> response also responded to the application of TRP agonist. These results suggest that the TRP channel is a potent candidate of central chemosensing molecules.

髓质含有对维持血气和pH稳态重要的中央化学敏感细胞（CRC）。为了鉴定内在的CRC，我们测量了细胞内Ca^<2+>和H^+的反应，以及大鼠原代培养的髓细胞短暂暴露（秒级）于高碳酸酸中毒的膜电位。在富含胶质细胞的培养物中，细胞内酸化先于高碳酸酸中毒诱导的Ca^2+反应，而与细胞外pH无关。TRP通道阻断剂可减弱高碳酸酸中毒诱导的Ca^2+反应。表现出高碳酸血症诱导的Ca^2+反应的细胞亚群也对TRP激动剂的应用产生了反应。这些结果表明，TRP通道是一个潜在的候选人的中央化学传感分子。

项目成果

TRP channels are involved in mediating hypercapnic Ca2+ responses in rat glia-rich medullary cultures independently of extracellular pH

TRP 通道参与介导富含胶质细胞的大鼠髓质培养物中的高碳酸钙反应，与细胞外 pH 无关

• 发表时间: 2010
• 期刊: Cell calcium 48
• 作者: Hirata Y;Oku Y
• 通讯作者: Oku Y

TRP channels are involved in mediating hypercapnic Ca2+ responses in rat glia-rich medullary cultures independent of extracellular pH

• DOI: 10.1016/j.ceca.2010.07.006
• 发表时间: 2010-08-01
• 期刊: CELL CALCIUM
• 影响因子: 4
• 作者: Hirata, Yutaka;Oku, Yoshitaka
• 通讯作者: Oku, Yoshitaka