The elucidation of molecular basis on mechanisms for chemosensitive respiratory regulation

髓质含有中央化学敏感细胞（CRC），对维持血气和pH稳态很重要。为了确定内在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质细胞对短暂暴露（秒级）高碳酸酸中毒的膜电位。在富含胶质细胞的培养中，细胞内酸化先于高碳酸酸中毒诱导的Ca^<2+>反应，与细胞外ph无关。TRP通道阻滞剂减弱了高碳酸酸中毒诱导的Ca^<2+>反应。表现出高碳酸酸中毒诱导的Ca^<2+>反应的细胞亚群也对TRP激动剂的应用有反应。这些结果表明TRP通道是中心化学传感分子的有力候选。

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.