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 (I_SAH) with a decay time constant ranging from 0.5 to 2 s. TheI_SAH was due to an increase in membrane conductance to K⁺ because its reversal potential was approximately equal to the Nernst potential for K⁺. TheI_SAH was reversibly blocked by removal of external Ca²⁺ or by Ca²⁺ antagonists. A Ca²⁺ ionophore, A23187, produced an outward current which was similar to theI_SAH. TheI_SAH was resistant to tetraethylammonium and depressed by Ba²⁺, whereas it was not affected by Cs⁺ and 4-aminopyridine. TheI_SAH was initially augmented and subsequently depressed by apamin (1–10 nM) and (+)-tubocurarine (100–600 M). It is concluded that theI_SAH 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.