Two components of Ca-dependent potassium current in identified neurons of Aplysia californica.
Outward tail currents measured in Aplysia neurones after termination of depolarizing voltage-clamp pulses consist of rapidly decaying voltage-dependent K currents and slow tail currents of much slower time course. The rapidly decaying voltage-dependent tail currents were blocked with aminopyridines, and measurements of the slow tail currents were made following decay of any residual rapid tail currents. The slow tail current exhibited two components of differing sensitivity to externally applied tetraethylammonium (TEA) ions. In some neurones of the abdominal ganglion (L-2, L-4), virtually all of the slow tail current was resistant to blockage by TEA, while in others (L-3, L-6) 80% or more of the slow tail current was blocked by low TEA concentrations (KD less than 1 mM), the remaining slow tail current being resistant to TEA. This TEA-resistant slow tail current was identified as a K current because it reversed near the K equilibrium potential (EK), the reversal potential was shifted by changes in the external K concentration, and it could be blocked by injection of Cs+. It was abolished by replacement of external Ca2+ by Co2+ or Ba2+, by addition of Cd2+, or by injection of EGTA, and thus determined to be a Ca-dependent current. Intracellular injection of TEA or external application of aminopyridine or apamine had little or no effect on the TEA-resistant slow tail current. Quinidine reduced the TEA-sensitive, but not the TEA-resistant current. Both the TEA-sensitive and the TEA-resistant components of the slow tail current exhibited similar time courses of decay.(ABSTRACT TRUNCATED AT 250 WORDS)
J W
JW
Deitmer
R
R
Eckert
D000818:Animals; D001030:Apamin / Q000494:pharmacology; D001048:Aplysia; D002118:Calcium / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D004351:Drug Resistance; D004553:Electric Conductivity; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000378:metabolism*; D011188:Potassium / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011802:Quinidine / Q000494:pharmacology; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013997:Time Factors
D007473:Ion Channels; D013757:Tetraethylammonium Compounds; D001030:Apamin; D019789:Tetraethylammonium; D011802:Quinidine; D011188:Potassium; D002118:Calcium