Abstract

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°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°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°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.

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