Chloride transport blockers inhibit the chloride-dependent glutamate binding to rat brain membranes.

The effects of a series of chloride transport blockers (ethacrynate, furosemide, torasemide, 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene and diphenylcarboxylate) on Cl(-)-dependent L-[3H]glutamate (Glu) binding were tested in rat brain membranes, Cl-transport blockers inhibit the Ca2+/Cl(-)-induced increase in L-[3H]Glu binding, some of them without affecting the Ca2+/Cl(-)-independent L-[3H]Glu binding. Increasing the medium osmolarity by augmenting the sucrose concentration also inhibited the Ca2+/Cl(-)-induced increase in L-[3H]Glu binding. The effects of both sucrose and Cl-transport blockers were not additive, suggesting that they acted on the same type of mechanism. We recently suggested that L-[3H]Glu binding to brain membranes corresponds to Glu uptake in membrane vesicles. Therefore we propose that the Cl-transport blockers inhibit a Cl(-)-dependent Glu accumulation into these vesicles.