Abstract

I AHP is a calcium dependent potassium current that underlies slow afterhyperpolarizations following action potentials in bullfrog sympathetic ganglion neurons. The decay rate of I AHP increases with increasing calcium loads. This effect was found not to be due to mobilization on intracellular calcium from ryanodine and caffeine sensitive stores. The relation is not affected by ryanodine at concentrations that block mobilization in the presence of caffeine, a drug that enhances mobilization of those stores. Nor does the relation seem to be due to a reduction of the driving force of the Na Ca exchange process. The relation between decay rate and calcium load persists when Na + is replaced by Li +. Our results suggest that Na Ca exchange and mobilization of intracellular calcium normally have little influence in determining the time course of I AHP in these neurons.

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