Ballanyi K, Mückenhoff K, Bellingham M C, Okada Y, Scheid P, Richter D W
II. Physiologisches Institut, Universität Göttingen, Germany.
Neuroreport. 1994 Dec 30;6(1):33-6. doi: 10.1097/00001756-199412300-00010.
Intracellular pH (pHi) and membrane potential (Em) were measured in vivo in expiratory neurones and glial cells in the medulla of anaesthetized cats using double-barrelled H(+)-sensitive microelectrodes. In glial cells, stimulation of spinal pathways evoked a depolarization of up to 12 mV amplitude and an increase of pHi (7.25 +/- 0.15) by maximally 0.1 pH unit. IN expiratory neurones, pHi (7.15 +/- 0.18) fell by up to 0.2 pH unit during inspiratory inhibition. In axons of expiratory neurones, pHi remained unaffected during rhythmic action potential discharges. We suggest that the glial alkalinization is due to activation of Na+/HCO3- cotransport, whereas the neuronal acidification is caused by efflux of HCO3- via receptor-coupled anion channels.
使用双管氢离子敏感微电极在麻醉猫延髓的呼气神经元和神经胶质细胞中体内测量细胞内pH值(pHi)和膜电位(Em)。在神经胶质细胞中,刺激脊髓通路可诱发高达12 mV幅度的去极化,并且pHi(7.25±0.15)最大增加0.1个pH单位。在呼气神经元中,吸气抑制期间pHi(7.15±0.18)下降高达0.2个pH单位。在呼气神经元的轴突中,有节律的动作电位发放期间pHi保持不受影响。我们认为神经胶质细胞碱化是由于Na+/HCO3-共转运的激活,而神经元酸化是由HCO3-通过受体偶联阴离子通道外流引起的。