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The effects of the voltage-dependent Ca2+ inward current (ICa) on gamma-aminobutyric acid (GABA)-induced Cl- current (ICl) in isolated frog sensory neurones were examined using the "concentration clamp" technique, an approach which combines internal perfusion by a suction pipette with a rapid external solution change method. A preceding ICa suppressed the GABA-activated ICl. While the inhibition was not influenced by changes of membrane potential between -40 and -100 mV, it was reduced when the internal EGTA concentration was increased. A preceding ICa shifted the GABA dose-response curve to the right without affecting the maximum current or the Hill coefficient (n = 2). Inhibition of the GABA-activated ICl by ICa showed a recovery in a single exponential manner, the time constant of which depended upon the extent of Ca2+ influx. At a low temperature (10 degrees C), however, the recovery from Ca2+-mediated inhibition was only slight. We conclude that, as a result of the voltage-dependent Ca2+ influx, a subsequent increase of intracellular Ca2+ concentration modulates the GABA-gated ICl in the soma membrane. Possible mechanisms are discussed.

Modulation of the .GAMMA.-aminobutyric acid-gated chloride current by intracellular calcium in frog sensory neurones.