The Journal of Neurophysiology Vol. 79 No. 5 May 1998, pp. 2338-2344
Copyright ©1998 The American Physiological Society

Voltage-Gated and Ca²⁺-Activated Conductances Mediating and Controlling Graded Electrical Activity in Crayfish Muscle

Alfonso Araque¹, Alain Marchand², and Washington Buño¹

¹ Instituto Cajal, Consejo Superior de Investigaciones Científicas, E-28002 Madrid, Spain; and ² Laboratoire de Neurobiologie et Mouvements, Centre National de la Recherche Scientifique, F-13402 Marseille, France

Araque, Alfonso, Alain Marchand, and Washington Buño. Voltage-gated and Ca²⁺-activated conductances mediating and controlling graded electrical activity in crayfish muscle. J. Neurophysiol. 79: 2338-2344, 1998. Crayfish opener muscle fibers provide a unique preparation to quantitatively evaluate the relationships between the voltage-gated Ca²⁺ (I_Ca) and Ca²⁺-activated K⁺ (I_K(Ca)) currents underlying the graded action potentials (GAPs) that typify these fibers. I_Ca, I_K(Ca), and the voltage-gated K⁺ current (I_K) were studied using two-electrode voltage-clamp applying voltage commands that simulated the GAPs evoked in current-clamp conditions by 60-ms current pulses. This methodology, unlike traditional voltage-clamp step commands, provides a description of the dynamic aspects of the interaction between different conductances participating in the generation of the natural GAP. The initial depolarizing phase of the GAP was due to activation of the I_Ca on depolarization above approximately 40 mV. The resulting Ca²⁺ inflow induced the activation of the fast I_K(Ca) (<3 ms), which rapidly repolarized the fiber (<6 ms). Because of its relatively slow activation, the contribution of I_K to the GAP repolarization was delayed. During the final steady GAP depolarization I_Ca and I_K(Ca) were simultaneously activated with similar magnitudes, whereas I_K aided in the control of the delayed sustained response. The larger GAPs evoked by higher intensity stimulations were due to the increase in I_Ca. The resulting larger Ca²⁺ inflow increased I_K(Ca), which acted as a negative feedback that precisely controlled the fiber's depolarization. Hence I_K(Ca) regulated the Ca²⁺-inflow needed for the contraction and controlled the depolarization that this Ca²⁺ inflow would otherwise elicit.

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