Depolarization shifts the voltage dependence of cardiac sodium channel and calcium channel gating charge movements

1996 ◽  
Vol 431 (6) ◽  
pp. 895-904 ◽  
Author(s):  
Ira R. Josephson
Keyword(s):  
Calcium Channel ◽  
Sodium Channel ◽  
Voltage Dependence ◽  
Channel Gating ◽  
Gating Charge ◽  
Cardiac Sodium Channel ◽  
Charge Movements

scholarly journals Resting Potential–dependent Regulation of the Voltage Sensitivity of Sodium Channel Gating in Rat Skeletal Muscle In Vivo

2005 ◽  
Vol 126 (2) ◽  
pp. 161-172 ◽  
Author(s):  
Gregory N. Filatov ◽  
Martin J. Pinter ◽  
Mark M. Rich
Keyword(s):  
Skeletal Muscle ◽  
Sodium Channel ◽  
Voltage Dependence ◽  
Channel Gating ◽  
Resting Potential ◽  
Sodium Currents ◽  
Fast Inactivation ◽  
Adult Skeletal Muscle ◽  
Muscle Excitability

Normal muscle has a resting potential of −85 mV, but in a number of situations there is depolarization of the resting potential that alters excitability. To better understand the effect of resting potential on muscle excitability we attempted to accurately simulate excitability at both normal and depolarized resting potentials. To accurately simulate excitability we found that it was necessary to include a resting potential–dependent shift in the voltage dependence of sodium channel activation and fast inactivation. We recorded sodium currents from muscle fibers in vivo and found that prolonged changes in holding potential cause shifts in the voltage dependence of both activation and fast inactivation of sodium currents. We also found that altering the amplitude of the prepulse or test pulse produced differences in the voltage dependence of activation and inactivation respectively. Since only the Nav1.4 sodium channel isoform is present in significant quantity in adult skeletal muscle, this suggests that either there are multiple states of Nav1.4 that differ in their voltage dependence of gating or there is a distribution in the voltage dependence of gating of Nav1.4. Taken together, our data suggest that changes in resting potential toward more positive potentials favor states of Nav1.4 with depolarized voltage dependence of gating and thus shift voltage dependence of the sodium current. We propose that resting potential–induced shifts in the voltage dependence of sodium channel gating are essential to properly regulate muscle excitability in vivo.

scholarly journals Sodium channel gating currents in frog skeletal muscle.

1983 ◽  
Vol 82 (5) ◽  
pp. 679-701 ◽  
Author(s):  
D T Campbell
Keyword(s):  
Skeletal Muscle ◽  
Sodium Channel ◽  
Time Course ◽  
Channel Gating ◽  
Total Charge ◽  
Charge Movement ◽  
Frog Skeletal Muscle ◽  
Gating Currents ◽  
Gating Mechanism ◽  
Charge Movements

Charge movements similar to those attributed to the sodium channel gating mechanism in nerve have been measured in frog skeletal muscle using the vaseline-gap voltage-clamp technique. The time course of gating currents elicited by moderate to strong depolarizations could be well fitted by the sum of two exponentials. The gating charge exhibits immobilization: at a holding potential of -90 mV the proportion of charge that returns after a depolarizing prepulse (OFF charge) decreases with the duration of the prepulse with a time course similar to inactivation of sodium currents measured in the same fiber at the same potential. OFF charge movements elicited by a return to more negative holding potentials of -120 or -150 mV show distinct fast and slow phases. At these holding potentials the total charge moved during both phases of the gating current is equal to the ON charge moved during the preceding prepulse. It is suggested that the slow component of OFF charge movement represents the slower return of charge "immobilized" during the prepulse. A slow mechanism of charge immobilization is also evident: the maximum charge moved for a strong depolarization is approximately doubled by changing the holding potential from -90 to -150 mV. Although they are larger in magnitude for a -150-mV holding potential, the gating currents elicited by steps to a given potential have similar kinetics whether the holding potential is -90 or -150 mV.

A model of sodium channel inactivation based upon the modulated blocker

1983 ◽  
Vol 219 (1217) ◽  
pp. 423-438 ◽  
Keyword(s):  
Sodium Channel ◽  
Time Constant ◽  
Voltage Dependence ◽  
Physical Principle ◽  
Membrane Voltage ◽  
Displacement Current ◽  
Channel Inactivation ◽  
Gating Charge ◽  
Sodium Channel Inactivation ◽  
Activation Characteristic

An attempt is made to model sodium channel inactivation based upon real physical processes. The principle involved, which is supported by calculation and by direct appeal to experimental results, is that the gating dipole reversal or gating charge transfer that occurs when the channel is activated, markedly modulates the electrical properties of charged groups at the channel ends. Four examples of possible mechanisms that lead to channel inactivation are described. The simple four-state model that results is able to predict: ( а ) the steep voltage dependence of the equilibrium inactivation characteristic without the presence of any appreciable displacement current associated with inactivation; ( b ) the negative shift in membrane voltage of the equilibrium inactivation characteristic relative to the activation characteristic; ( c ) the bell-shaped dependence of inactivation time constant on membrane voltage; ( d ) the similarity of the membrane voltage dependence of the time constant of recovery from inactivation, to that of inactivation itself. A brief discussion of a model for sodium channel activation based upon the same physical principle is included.

scholarly journals Modulation of Cardiac Sodium Channel Gating by Protein Kinase A Can Be Altered by Disease-linked Mutation

2003 ◽  
Vol 278 (47) ◽  
pp. 46718-46726 ◽  
Author(s):  
Michihiro Tateyama ◽  
Ilaria Rivolta ◽  
Colleen E. Clancy ◽  
Robert S. Kass
Keyword(s):  
Protein Kinase ◽  
Sodium Channel ◽  
Protein Kinase A ◽  
Channel Gating ◽  
Cardiac Sodium Channel ◽  
Kinase A
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