Reprimed charge movement in skeletal muscle fibres.

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Abstract
The 3 intracellular micro-electrode voltage-clamp technique was used to study the recovery of membrane charge movement in semitendinosus muscles of Rana pipiens. Muscles were placed in a hypertonic depolarizing solution to inactivate voltage dependent charge movement. Tetrodotoxin and tetraethylammonium ions (TEA+) were present to block voltage dependent ionic conductances. Rb+ and SO42- were present to reduce inward rectification and leakage conductance. The recovery (repriming) of membrane charge movement was studied following hyperpolarizing pulses from a holding potential of -20 mV to membrane potentials from -30 to -140 mV for durations of 2-100 s. The reprimed charge movement measured as the difference in membrane current required for identical voltage steps before and after long duration hyperpolarizing pulses was a linear function of membrane potential and symmetrical in shape. Reprimed charge is, therefore, simply the result of an increase in the linear capacitance of the fiber. The mean value of the percent increase in capacitance for repriming at -100 mV was 12.3 .+-. 1.7% (SE of mean) for 25 s duration pulses and 27.8 .+-. 2.9% for 100 s duration pulses. If these data are corrected to the steady state and the surface contribution subtracted, the mean increase in volume capacity is 40.3 .+-. 3.6% (n = 21) for fibers with a mean diameter of 51 .+-. 4 .mu.m. The increase in capacity can arise either by an increase in the transverse tubular length constant (.lambda.T) or by gaining electrical access to additional linear capacitance within the fiber volume. If the capacitance arises solely from the transverse tubular system, the value of .lambda.T before repriming can be no larger than 20 .mu.m in order to explain the observed increase in volume capacity. A value of .lambda.T as small as this seems unlikely. The observation that reprimed charge is simply the result of an increase in linear capacitance is not consistent with the hypothesis that it is a gating mechanism for the activation of contraction.