A calcium‐activated chloride current generates the after‐depolarization of rat sensory neurones in culture.

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Abstract
Neurons from the dorsal root ganglia of 1 day old rat pups were grown in dissociated culture and voltage clamped using patch electrodes for whole-cell recording. The pipettes were filled with either 140 mM-KCl or CsCl. Depolarizing voltage jumps activated net inward Ca currents in all neurons, which in a subpopulation of 46% were followed by slowly decaying inward tail currents accompanied by large increases in membrane conductance. During voltage jumps to membrane potentials more positive than 0 mV the inward Ca current was contaminated by a slow outward relaxation only in those neurons with slow inward tail currents. The availability curve for the slow inward tail current was U shaped, with a peak at .apprx. +5 mV in medium containing 2.5 mM-Ca2+; further depolarization reduced the amplitude of the tail current. During perfusion with Ca-free solution or in the presence of the Ca-channel blockers Cd or Co or on substitution of Ba for Ca, the slow inward tail currents and outward relaxations were reversibly blocked. The reversal potential of the slow inward tail current, measured using a twin-pulse protocol, was .apprx. -10 mV. Replacement of Na by tetraethylammonium (TEA) did not reduce the slow inward tail current, nor change its reversal potential. Reduction of the extracellular chloride activity produced a large increase in the amplitude of the slow inward tail current suggesting an increase in permeability to anions. This conductance, which behaves as though activated by prior or concurrent Ca entry triggered by membrane potential depolarization, is referred to as ICl(Ca). The activation and deactivation kinetics of ICl(Ca) are complex: envelope experiments measuring peak tail current amplitude revealed activation to be described by a single exponential function, of time constant .apprx. 100 ms at -10 to +8 mV. The integral of the tail currents increased with the duration of depolarizing pre-pulses suggesting accumulation of intracellular Ca. The decay of tail currents activated by short depolarizing voltage jumps was described by a single exponential function of time constant .apprx. 200 ms at -60 m V; more complex decay kinetics were recorded following activation by voltage jumps of duration > 60 ms. Tail current decay was voltage sensitive, becoming faster with hyperpolarization and increasing e-fold/ 120 mV change in membrane potential.