Calcium-dependent slow outward current in visceral primary afferent neurones of the rabbit.

Slow outward currents were recorded from voltage-clamped neurones in nodose ganglia excised from rabbits. In the majority of Type C neurones, a short depolarizing command pulse evoked a slow outward tail current (ISAH) with a decay time constant ranging from 0.5 to 2 s. The ISAH was due to an increase in membrane conductance to K+ because its reversal potential was approximately equal to the Nernst potential for K+. The ISAH was reversibly blocked by removal of external Ca2+ or by Ca2+ antagonists. A Ca2+ ionophore, A23187, produced an outward current which was similar to the ISAH. The ISAH was resistant to tetraethylammonium and depressed by Ba2+, whereas it was not affected by Cs+ and 4-aminopyridine. The ISAH was initially augmented and subsequently depressed by apamin (1-10 nM) and (+)-tubocurarine (100-600 microM). It is concluded that the ISAH in visceral primary neurones may be due to a long-lasting increase in K+ conductance caused by an increase in the concentration of intracellular Ca2+, resulting from Ca2+ entry during the depolarizing command pulse.