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pubmed:abstractText |
Depolarizing voltage-clamp pulses elicit a triphasic series of tail currents (phase I, II and III) in Aplysia burst-firing neurones L2-L6. The sequence and time course of the tail currents resemble slow changes in membrane potential which follow bursts in the unclamped cell. The phase II tail current is an inward current with a time course similar to that of the depolarizing after-potential (d.a.p.) which follows bursts in the unclamped cell. The phase II tail current is suppressed by depolarizing pulses which approach ECa, is blocked by Ca2+ current antagonists (Co2+ and Mn2+), and is blocked by intracellular injection of EGTA. The phase II tail current is not blocked by agents which block Na+-dependent action potentials, the Na+-Ca2+ exchange pump, or the Na+-K+ exchange pump. The phase II tail current is not blocked by the elimination of large outward K+ currents which can lead to extracellular K+ accumulation. Thus, the phase II tail current is not generated by any of these processes. The phase II tail current is reduced by about 60% following substitution of tetramethylammonium (TMA+) for external Na+, but is unaffected by reducing external Cl-. The phase II tail current is distinct from a persistent inward Ca2+ current which underlies the negative resistance region of the steady-state current--voltage relation of bursting cells. The persistent inward current is only slightly reduced by TMA+ substitution for Na+, and is enhanced by EGTA injection. Injection of Ca2+ into Aplysia bursting cells elicits a biphasic (inward-outward) current. The inward current can be observed in isolation after blocking the outward component (Ca2+-activated K+ current) with 50 mM-external tetraethylammonium. The Ca2+-elicited inward current has a reversal potential near -22 mV, and is non-selective for Na+, K+ and Ca2+. The reversal potential is unaffected by changes in Cl- and pH. The Ca2+- activated conductance is apparently voltage independent. We propose that the phase II tail current, and hence the d.a.p., is due to the Ca2+-dependent activation of a voltage-independent non-specific cationic conductance. This conductance participates in generating the depolarizing phase of bursting pace-maker activity.
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