COUNTERTRANSPORT OF POTASSIUM BY THE GLUTAMATE UPTAKE CARRIER IN GLIAL-CELLS ISOLATED FROM THE TIGER SALAMANDER RETINA

1. To investigate the transport of potassium on the glutamate uptake c arrier, the glutamate uptake current in isolated retinal Muller cells was monitored by whole-cell clamping, while measuring changes of potas sium concentration outside the cells ([K+](o)) with an ion-sensitive m icroelectrode. 2. Activating glutamate uptake led to an accumulation o f potassium outside the cells, consistent with the hypothesis, based o n less direct evidence, that the glutamate uptake carrier transports p otassium out of the cell. 3. The glutamate-evoked rise of [K+](o) show ed the pharmacology and sodium dependence of glutamate uptake. 4. The rise in [K+](o) was proportional to the uptake current flowing between 0 and -80 mV, implying that the ratio of K+ transported to charge tra nsported by the uptake carrier is constant over this voltage range. Th e K+ to charge transport ratio was the same for uptake of D-aspartate and L-glutamate. 5. By clamping cells with pipettes containing solutio ns of different [K+], the dependence of the glutamate and aspartate up take currents on intracellular [K+] was determined. L- and D-aspartate transport showed a smaller maximum uptake current (I-max), and a smal ler apparent Michaelis constant (K-m) for activation by intracellular K+, than did L-glutamate transport. The ratio of I-max to K-m was the same for these three analogues, a result which can be predicted from s imple models of the carrier's operation. 6. Fully activating glutamate uptake in Muller cells in the intact retina would produce a K+ load i nto the extracellular space of about 0.6 mM s(-1). Suppression of glut amate release from photoreceptors by light will reduce K+ efflux from Muller cells in the outer retina; this may contribute to the light-evo ked fall of [K+](o) observed in the outer retina, and thus contribute to shaping the electroretinogram.