Enhancement of glutamate uptake transport by CO2/bicarbonate in the leech giant glial cell

Glutamate uptake into glial cells via the excitatory amino acid transporter (EAAT) is accompanied by an influx of sodium and acid equivalents into the cells. The sodium-bicarbonate cotransport (NBC) in glial cells moves sodiu m and base equivalents across the glial membrane in both directions. We hav e studied possible interactions between these two electrogenic transporters in the giant glial cell of isolated ganglia of the leech Hirudo medicinali s. Changes in membrane potential, membrane current, intracellular sodium, a nd intracellular pH evoked by aspartate (1 mM), an EAAT agonist, were measu red both in the absence and in the presence of CO2/bicarbonate. When 5% CO2 and 24 mM bicarbonate was added to the saline (at constant pH 7.4), the as partate-induced membrane current was increased, while the change in intrace llular sodium was decreased. The acid influx evoked by aspartate was enhanc ed by CO2/bicarbonate but, because of the increased intracellular CO2/bicar bonate-dependent buffering power, the change in intracellular pH was decrea sed. 4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS, 0.5 mM), whi ch inhibits the NBC, reversed the effects of CO2/bicarbonate on the asparta te-induced current and pH change. Our results suggest that the NBC helps co unteract dissipation of the sodium and the acid-base gradients induced by t he EAAT, enhancing the rate and capacity of glutamate uptake by glial cells . (C) 2000 Wiley-Liss, Inc.