Quisqualate‐sensitive, chloride‐dependent transport of glutamate into rat brain synaptosomes

Abstract

A chloride‐dependent transport process for glutamate has been identified in partially purified rat brain synaptosomes. This process shares many characteristics with the chloride‐dependent sequestration process for glutamate in brain sonicates, which was previously thought to represent a quisqualate receptor, such as sensitivity to specific inhibitors and regulation by anions. Increases the concentrations of chloride led to and increase in the apparent V_max without affecting the K_T. Synaptosomes preincubated with [³H]‐L‐glutamate exhibit an efflux of the radiolabel, which was stimulated by a substrate for the carrier in the incubating medium, indicating the bidirectional nature of the transport. The chloride‐dependent transfer process is restricted to the brain, and regional and developmental profiles clearly distinguish it from the sodium‐dependent high‐affinity uptake process for glutamate. Nevertheless, the effects of excitotoxic lesions strongly suggest a neuronal localization of the chloride‐dependent transport.