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The previous paper described a slow depolarizing tail current, ID, and a slow hyperpolarizing tail current, IH, that are activated by action potentials and by brief depolarizing pulses in Aplysia neurone R15. ID and IH are necessary for the generation of bursting pace-maker activity in this cell. In this paper, the voltage and ion dependence of ID and IH are studied in an effort to determine the charge carriers for the two currents. When the slow currents are activated by brief depolarizing pulses delivered under voltage clamp in normal medium, an increase in the size of the pulse of 5-10 mV is usually sufficient to bring about full activation of ID. The apparent threshold in normal medium is approximately -20 mV. In medium in which K+ channels are blocked, full activation of an inward tail current that resembles ID requires increasing the pulse amplitude by only 1-2 mV. In contrast, IH is activated in a graded fashion over a 40 mV range of pulse amplitudes. After activating the currents with action potentials or with supramaximal pulses, ID remains an inward current and IH an outward current over a range of membrane potentials spanning -20 to -120 mV. In normal medium, ID is dependent on both extracellular Na+ concentration ( [Na+]o) and extracellular Ca2+ concentration ( [Ca2+]o). When K+ channels are blocked, ID can be supported by either [Na+]o or [Ca2+]o. IH depends only on [Ca2+]o as long as [Na+]o is at least 50 mM. Neither ID nor IH is decreased by decreasing the K+ gradient or by application of K+ channel blockers. These treatments increase somewhat the apparent amplitude of ID, probably by unmasking it from the large K+ tail current that follows the depolarizing pulse. A direct comparison in the same cell of the tetraethylammonium sensitivity of IH and of the Ca2+-activated K+ current demonstrates that these two currents flow through separate and distinct populations of channels. We conclude that in R15, ID arises in response to the triggering of an axonal action potential which in turn, through an as yet unknown mechanism, causes an increased influx of Na+ and/or Ca2+. We conclude that the apparent outward current IH, which is responsible for the interburst hyperpolarization in a normally bursting R15, in fact arises from a decrease in a resting inward Ca2+ current, possibly as the result of Ca2+-induced inactivation of Ca2+ channels.
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