Characterization of the membrane ion currents of a model molluscan muscle, the accessory radula closer muscle of Aplysia californica. II. Depolarization-activated K currents.
1. The accessory radula closer (ARC) muscle of Aplysia californica and its innervation is a model preparation for the study of the neural and cellular mechanisms of behavioral plasticity. Much of the plasticity is mediated by release of neurotransmitters and peptide cotransmitters that modulate contractions of the muscle. Preliminary to investigating the cellular mechanisms of action of these modulators, we have characterized the major membrane ion currents present in the unmodulated ARC muscle and their likely roles in normal contraction. We have studied single dissociated but functionally intact ARC muscle fibers under voltage clamp. This is the second of three papers describing this work. In the preceding paper we described the electrophysiological properties of the fibers at hyperpolarized voltages, and characterized the two major hyperpolarized-activated currents present, a classical inwardly rectifying K current and a Cl current induced by elevated intracellular Cl-. 2. In this paper we dissect the large outward current that becomes activated when the fibers are depolarized above -50 or -40 mV. We find that this current consists of two major depolarization-activated K currents, a fast transient "A"-type current and a slower maintained delayed rectifier, with perhaps a small component of Ca(2+)-activated K current. 3. The A current begins to activate with voltage steps above -50 or -40 mV. It activates in milliseconds, then inactivates virtually completely within 100-200 ms. It is fully available for activation below -80 mV, and almost completely inactivated above -40 mV. It is Ca2+ independent, half-maximally blocked by approximately 3 mM 4-aminopyridine (4-AP) but only 460 mM tetraethylammonium (TEA). 4. The delayed rectifier both activates and inactivates more slowly and more positive than the A current. Thus it begins to activate only above -30 or -20 mV; it activates in tens of milliseconds, then inactivates incompletely over several seconds; it is fully available below -70 mV and inactivated above 0 mV. It is Ca2+ independent, half-maximally blocked by 10 mM TEA and 3-10 mM 4-AP. 5. In the following paper we describe a depolarization-activated Ca current that underlies the K currents and most likely provides Ca2+ necessary for contraction of the muscle. By activating simultaneously with the Ca current, the K currents serve to prevent spikes, so that the depolarization is confined to a range where small voltage changes provide fine control over a wide range of contraction strengths.
Brezina
V
V
Department of Physiology and Biophysics, Mount Sinai School of Medicine, New York 10029.
Evans
C G
CG
Weiss
K R
KR
D000818:Animals; D001048:Aplysia; D015220:Calcium Channels / Q000502:physiology; D004558:Electric Stimulation; D005247:Feeding Behavior / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D009046:Motor Neurons / Q000502:physiology*; D009119:Muscle Contraction / Q000502:physiology; D009132:Muscles / Q000294:innervation*; D009415:Nerve Net / Q000502:physiology*; D009469:Neuromuscular Junction / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*
D015220:Calcium Channels; D015221:Potassium Channels