Abstract

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.

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