Enhancement of glutamate uptake transport by CO(2)/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 sodium and base equivalents across the glial membrane in both directions. We have studied possible interactions between these two electrogenic transporters in the giant glial cell of isolated ganglia of the leech Hirudo medicinalis. Changes in membrane potential, membrane current, intracellular sodium, and intracellular pH evoked by aspartate (1 mM), an EAAT agonist, were measured both in the absence and in the presence of CO(2)/bicarbonate. When 5% CO(2) and 24 mM bicarbonate was added to the saline (at constant pH 7.4), the aspartate-induced membrane current was increased, while the change in intracellular sodium was decreased. The acid influx evoked by aspartate was enhanced by CO(2)/bicarbonate but, because of the increased intracellular CO(2)/bicarbonate-dependent buffering power, the change in intracellular pH was decreased. 4,4'-Diisothiocyanatostilbene-2, 2'-disulfonic acid (DIDS, 0.5 mM), which inhibits the NBC, reversed the effects of CO(2)/bicarbonate on the aspartate-induced current and pH change. Our results suggest that the NBC helps counteract dissipation of the sodium and the acid-base gradients induced by the EAAT, enhancing the rate and capacity of glutamate uptake by glial cells.