title: Characterization of the membrane ion currents of a model molluscan muscle, the accessory radula closer muscle of Aplysia californica. III. Depolarization-activated Ca current.
abstract: 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 due to modulation of contractions of the muscle by a variety of neurotransmitters and peptide cotransmitters. Preliminary to investigating the cellular mechanisms of this modulation, 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 last of three papers describing this work. In the first paper we characterized two currents prominent at hyperpolarized voltages, a classical inwardly rectifying K current and a Cl current induced by elevated intracellular Cl-. In the second paper we examined two large outward K currents activated at more depolarized voltages, an "A" current and a delayed rectifier. 2. In this paper, we describe an inward depolarization-activated Ca current that underlies and is normally completely masked by the K currents and is revealed when they are blocked. 3. The Ca current begins to activate above -40 or -30 mV. It is fully available for activation at voltages more negative than -60 mV. It activates in milliseconds, then inactivates relatively slowly with maintained depolarization. The current is larger and inactivates slower when it is carried by Ba2+ rather than Ca2+. The inactivation is current rather than voltage dependent. The current is blocked by Co2+, Cd2+, and with a characteristic time dependence, by the dihydropyridine Ca-channel antagonist nifedipine. 4. These properties of the current characterize it as a high-threshold, L-type Ca current. 5. This current most likely provides Ca2+ necessary for contraction of the ARC muscle.
authors.affiliation: Department of Physiology and Biophysics, Mount Sinai School of Medicine, New York 10029.
authors.forename: V
authors.initials: V
authors.lastname: Brezina
authors.forename: C G
authors.initials: CG
authors.lastname: Evans
authors.forename: K R
authors.initials: KR
authors.lastname: Weiss
mesh_terms: 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; D011930:Reaction Time / Q000502:physiology; D015222:Sodium Channels / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology*
chemical_list: D015220:Calcium Channels; D015221:Potassium Channels; D015222:Sodium Channels