Calcium dependence of A-currents in perfused Aplysia neurons.
Transient outward currents were studied in neurons in the visceral ganglion of Aplysia californica, using intracellular perfusion and voltage-clamp techniques. The early outward currents in response to depolarizations from holding potentials near -90 mV were activated in the range -60 to -20 mV, below the threshold for the delayed outward current. Resting inactivation of the early outward currents was removed by prehyperpolarizations in the range -130 to -70 mV. A-currents produced in this manner were blocked by external application of CoCl2 and augmented by increasing external Ca-concentration. They were also blocked by treatment with 4-aminopyridine. The currents were reduced by treatment with verapamil hydrochloride, further suggesting a role for calcium in the current-generating mechanism. A model with a fourth-power activation process and first-power inactivation process could fit the early outward currents reasonably well. The effect of application of Ca-free, cobalt-containing solution was modeled as a decrease in peak conductance and an increase in the time constants of activation and inactivation.
Junge
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D015761:4-Aminopyridine; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D001048:Aplysia; D002118:Calcium / Q000502:physiology*; D003035:Cobalt / Q000494:pharmacology; D005724:Ganglia / Q000502:physiology*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials; D009431:Neural Conduction; D011188:Potassium / Q000502:physiology*
D000631:Aminopyridines; D007473:Ion Channels; D003035:Cobalt; D015761:4-Aminopyridine; D011188:Potassium; D002118:Calcium