ANION CONDUCTANCE BEHAVIOR OF THE GLUTAMATE UPTAKE CARRIER IN SALAMANDER RETINAL GLIAL-CELLS

Glutamate uptake is driven by the cotransport of Na+ ions, the counter transport of K+ ions, and either the countertransport of OH- or the co transport of H+ ions. In addition, activating glutamate uptake carrier s has been shown to lead to activation of an anion conductance present in the carrier structure. Here we characterize the ion selectivity an d gating of this anion conductance. The conductance is small with Cl- as the permeant anion, but it is large with NO3- or ClO4- present, und ermining the earlier use of NO3- and ClO4- to suggest that OH- counter transport rather than H+ cotransport helps drive uptake. Activation of the anion conductance can be evoked by extra- or intracellular glutam ate and can occur even when glutamate transport is inhibited. By runni ng the carrier backward and detecting glutamate release with AMPA rece ptors in neurons placed near the glial cells, we show that anion flux is not coupled thermodynamically to glutamate movement, but OH-/H+ tra nsport is. The possibility that cell excitability is modulated by the anion conductance associated with glutamate uptake suggests a target f or therapeutic drugs to reduce glutamate release in conditions like ep ilepsy.