Abstract

Since activation of GABA A receptors is believed to open an associated Cl − channel, the intracellular Cl − activity (a i Cl) must be lower than that predicted from a passive distribution, to account for hyperpolarizing responses, or higher, to account for depolarizing responses. The physiological and pharmacological properties of the implied Cl − extruding and accumulating mechanisms have been investigated by direct measurements of a i Cl. A coupled K +-Cl − co-transport has been found in crayfish stretch receptor neurones and a predominating Cl −-HCO 3 − exchange in guinea pig vas deferens. From the different ionic mechanisms involved in Cl − extrusion and accumulation, it is proposed that drugs which affect Cl − transport mechanisms will reduce GABA responses of both polarities only if their action is via interference with the Cl − recognition site, but not if it is via interference with the co- or counter-ion recognition site.

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