Fig. 12. Proposed voltage shifts and transmembrane Na+/HCO−3 movements in astrocytes during kainate application in CO2/HCO−3-buffered saline.A, Model of KA-induced changes in membrane potential, [Na+]i, and Na+/HCO−3-cotransporter reversal potential in astrocytes. KA causes depolarization and increases [Na+]i (1). This is followed by Na+ pump stimulation leading to hyperpolarization and normalization of [Na+]i(2). The reversal potential of Na+/HCO−3 cotransport is altered by the changes in [Na+]i, illustrated by the hypothetical curves to the right. The upper trace shows the presumed changes in membrane potential (Em) resulting from KA application (1 mm for 1 min) (indicated bybars) (see also Bowman and Kimelberg, 1984; Kettenmann and Schachner, 1985; Backus et al., 1989). The middle trace shows the averaged KA-induced [Na+]i change of six representative cells. The lower trace shows changes in the reversal potential of Na+/HCO−3 cotransport (Erev), calculated from the average [Na+]i change in the middle trace (see Discussion). B, Proposed mechanism of the alkaline-acid transients seen in astrocytes resulting from KA application (1 mm for 1 min) (indicated bybars). The upper trace shows changes in the Erev (solid line). Superimposed on the Erev trace is the presumed change in Em induced by KA (dashed line) (see above). During the fast, KA-induced membrane depolarization,Em is more positive thanErev, favoring influx of Na+/HCO−3 and, therefore, intracellular alkalinization. During repolarization and hyperpolarization of the membrane, Em is more negative than Erev, because of the relatively slower recovery of [Na+]i, favoring efflux of Na+ and HCO−3 and intracellular acidification. The lower trace shows the KA-induced biphasic alkaline-acid shift in [H+]i averaged from six representative cells.