The reversal potential of Ca(2+)-activated Cl(-) currents indicates that chick sensory neurons accumulate intracellular Cl(-)

In order to establish the physiological role of the Ca(2+)-activated Cl(-) current (I(Cl(Ca))) of chick primary afferent neurons, I measured the reversal potential of this current using either the amphotericin perforated patch technique (that alters intracellular Cl(-)) or the gramicidin perforated patch technique (that does not perturb intracellular Cl(-)). In the amphotericin experiments at 35 degrees C, I(Cl(Ca)) reversed at the Cl(-) equilibrium potential (E(Cl)=-24 mV) set by the superfusate (147 mM Cl(-)) and the pipette solution (60 mM Cl(-)). In contrast, in the gramicidin experiments at 35 degrees C, I(Cl(Ca)) reversed at -42+/-2 mV, midway between E(Cl) of the solutions and E(Cl) expected if Cl(-) were passively distributed. Thus the gramicidin perforated patch technique monitors Cl(-) currents without perturbing intracellular Cl(-). Further, the data imply that chick dorsal root ganglia (DRG) neurons actively accumulate Cl(-). I(Cl(Ca)) reversed at the same potential (-46+/-3 mV) at 20 degrees C indicating that the non-equilibrium distribution of Cl(-) is maintained at the lower temperature. Thus, I(Cl(Ca)) is a depolarizing current that can contribute to the after-depolarization in chick DRG neurons and thereby alter Ca(2+) influx.