Divalent ion currents and the delayed potassium conductance in an Aplysia neurone.
1. In Na- and Ca-free external solutions, Sr or Ba (but not Mg) could act as carriers of inward current during action potentials in the neurone, R15 of the Aplysia abdominal ganglion. These action potentials exhibited a prolonged plateau phase, the duration of which was dependent on the concentration and species of divalent cation and activity of the neurone. 2. Depolarization of the soma membrane in Na-free Ba solution generated a prolonged, 'late' inward current the amplitude of which was dependent on the external Ba concentration. The Ba current was insensitive to tetrodotoxin but could be blocked by Mn2+ and Co2+ ions. 3. The peak current-voltage relation and threshold for activation of the late inward current was shifted to more negative potentials on replacement of Ca with Ba. The zero-current (reversal) potentials for both Sr and Ba were more negative than for Ca, indicating that the 'Ca' channel is less permeable to Sr2+ or Ba2+ ions than to Ca2+ ions. 4. Inactivation of the 'Ca' channel is slower in Ba than in Ca solution. The time course of Ba currents during a maintained depolarization of 2 sec could be reasonably described by the expression, I'Ba(t) = I'Ba (infinity) [1-exp(-t/tau M)]2exp(-t/tau H). 5. Time constants for activation (tau M) and inactivation (tau H) were voltage-dependent. In the range -10 to +30 mV, tau M varied from 15 to 5 msec and tau H from 2.0 to 0.5 sec (12 degrees C). Steady-state Ba conductance (corrected for inactivation) was voltage-dependent, increasing sigmoidally with depolarization to a maximum of approximately 12 microS at potentials beyond +15 mV. 6. Steady-state inactivation of Ba conductance (hBa(infinity)) varied with holding potential (VH). Conditioning holding potentials more negative than the resting potential (-40 to -50 mV) produced depression of Ba currents. Complete inactivation of Ba currents occurred at holding potentials more positive than 0 mV or with repetitive activation at frequencies greater than 1 Hz. 7. The divalent ions, Ba2+ and Sr2+, reversible depressed the total delayed K+ current at a rate dependent on the frequency of activation. Ba and Sr shifted the delayed K+ current-voltage curve to more positive voltages and depressed the delayed outward current at all membrane potentials. 8. Comparison of the effect of Ba on delayed K+ currents with those obtained in the presence of Mn2+ ions indicated that Ba2+ ions depress both the voltage-dependent and Ca-dependent components of the delayed K+ current. However, the mechanism by which Ba acts to inhibit the two components of the delayed K+ current appears to be different.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001048:Aplysia / Q000502:physiology*; D001464:Barium / Q000502:physiology; D002413:Cations, Divalent / Q000494:pharmacology; D004553:Electric Conductivity; D005724:Ganglia / Q000502:physiology; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000502:physiology*; D011188:Potassium / Q000502:physiology
D002413:Cations, Divalent; D007473:Ion Channels; D001464:Barium; D011188:Potassium