Schlue W R, Dörner R
Institut für Zoologie/Neurobiologie, Heinrich-Heine-Universität Düsseldorf, Germany.
Can J Physiol Pharmacol. 1992;70 Suppl:S278-85. doi: 10.1139/y92-273.
The pHi regulation from intracellular acidosis in the central nervous system appears to be mediated by mechanisms driven by the large inwardly directed Na+ gradient. The involvement of these mechanisms in pHi regulation of neurones and glial cells has been investigated in the leech central nervous system using ion-selective microelectrodes. For recovery from acidification, there appear to be three separate mechanisms: Na+/H+ exchange, Na(+)-dependent Cl-/HCO3- exchange, and Na+-HCO3- cotransport. All three mechanisms have a profound effect on the maintenance of pHi homeostasis in glial cells; whereas in leech neurones, as in other neuronal cells studied previously, the predominant mechanisms are Na+/H+ and Na(+)-dependent Cl-/HCO3- exchange. In addition to acid extrusion mechanisms we also found evidence for Na(+)-independent Cl-/HCO3- exchange. At alkaline pHi this exchanger may mediate some of the pHi recovery from intracellular alkalinization.
中枢神经系统中细胞内酸中毒引起的细胞内pH值（pHi）调节似乎是由内向的大Na+梯度驱动的机制介导的。利用离子选择性微电极，在水蛭中枢神经系统中研究了这些机制在神经元和神经胶质细胞pHi调节中的作用。对于从酸化中恢复，似乎有三种独立的机制：Na+/H+交换、Na+依赖的Cl-/HCO3-交换和Na+-HCO3-共转运。这三种机制对神经胶质细胞中pHi稳态的维持都有深远影响；而在水蛭神经元中，与之前研究的其他神经元细胞一样，主要机制是Na+/H+和Na+依赖的Cl-/HCO3-交换。除了酸排出机制外，我们还发现了Na+非依赖的Cl-/HCO3-交换的证据。在碱性pHi时，这种交换体可能介导细胞内碱化引起的部分pHi恢复。
