Duprat Fabrice, Lauritzen Inger, Patel Amanda, Honoré Eric
Institut de Pharmacologie Moléculaire et Cellulaire, Université de Nice-Sophia Antipolis, UMR CNRS 6097, Valbonne, France.
Trends Neurosci. 2007 Nov;30(11):573-80. doi: 10.1016/j.tins.2007.08.003. Epub 2007 Oct 22.
Specialized chemo- and nutrient-sensing cells share a common electrophysiological mechanism by transducing low O(2), high CO(2) and low glucose stimuli into a compensatory cellular response: the closing of background K(+) channels encoded by the K(2P) subunits. Inhibition of the TASK K(2P) channels by extracellular acidosis leads to an increased excitability of brainstem respiratory neurons. Moreover, hypoxic down-modulation of TASK channels is implicated in the activation of glomus cells in the carotid body. Stimulation of both types of cell leads to an enhanced ventilation and to cardiocirculatory adjustments. Differential modulation of TASK channels by acidosis and high glucose alters excitability of the hypothalamic orexin neurons, which influence arousal, food seeking and breathing. These recent results shed light on the role of TASK channels in sensing physiological stimuli.
专门的化学和营养感应细胞通过将低氧、高二氧化碳和低葡萄糖刺激转化为代偿性细胞反应,共享一种常见的电生理机制:关闭由K(2P)亚基编码的背景钾通道。细胞外酸中毒对TASK K(2P)通道的抑制会导致脑干呼吸神经元兴奋性增加。此外,TASK通道的低氧下调与颈动脉体中球细胞的激活有关。这两种类型细胞的刺激都会导致通气增强和心脏循环调节。酸中毒和高葡萄糖对TASK通道的差异调节会改变下丘脑食欲素神经元的兴奋性,这些神经元会影响觉醒、觅食和呼吸。这些最新结果揭示了TASK通道在感知生理刺激中的作用。