RELATION OF MEMBRANE PROPERTIES OF THE GIANT MUSCLE FIBER OF A BARNACLE TO INTERNAL IONIC COMPOSITION.
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Biomedical subjects
Publications and source records attributed to S HAGIWARA.
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Membrane properties of the giant muscle fiber of the barnacle Balanus nubilus were studied by controlling the ionic composition of the external and internal media. The resting potential decreases with increasing external K-concentration, [K(+)](out), and decreasing internal K-concentration, [K(+)](in), over a considerable range. Spike potentials are elicited when the internal calcium ions are removed, and the overshoot is determined by the ratio between [Ca(++)](out) and [K(+)](in) and not by the external or internal [Na(+)].
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Electrical properties of the muscle fiber membrane were studied in the barnacle, Balanus nubilus Darw. by using intracellular electrode techniques. A depolarization of the membrane does not usually produce an all-or-none spike potential in the normal muscle fiber even though a mechanical response is elicited. The intracellular injection of Ca(++)-binding agents (K(2)SO(4) and K salt of EDTA solution, K(3) citrate solution, etc.) renders the fiber capable of initiating all-or-none spikes. The overshoot of such a spike potential increases with increasing external Ca concentration, the increment for a tenfold increase in Ca concentration being about 29 mv. The threshold membrane potential for the spike and also for the K conductance increase shifts to more positive membrane potentials with increasing [Ca(++)](out). The removal of Na ions from the external medium does not change the configuration of the spike potential. In the absence of Ca(++) in the external medium, the spike potential is restored by Ba(++) and Sr(++) but not by Mg(++). The overshoot of the spike potential increases with increasing [Ba(++)](out) or [Sr(++)](out). The Ca influx through the membrane of the fiber treated with K(2)SO(4) and EDTA was examined with Ca(45). The influx was 14 pmol per sec. per cm(2) for the resting membrane and 35 to 85 pmol per cm(2) for one spike. From these results it is concluded that the spike potential of the barnacle muscle fiber results from the permeability increase of the membrane to Ca(++) (Ba(++) or Sr(++)).
Effects of monovalent cations and some anions on the electrical properties of the barnacle muscle fiber membrane were studied when the intra- or extracellular concentrations of those ions were altered by longitudinal intra-cellular injection. The resting potential of the normal fiber decreases linearly with increase of logarithm of [K(+)](out) and the decrement for a tenfold increase in [K(+)](out) is 58 mv when the product, [K(+)](out) .[Cl(-)](out), is kept constant. It also decreases with decreasing [K(+)](in) but is always less than expected theoretically. The deviation becomes larger as [K(+)](in) increases and the resting potential finally starts to decrease with increasing [K(+)](in) for [K(+)](in) > 250 mM. When the internal K(+) concentration is decreased the overshoot of the spike potential increases and the time course of the spike potential becomes more prolonged. In substituting for the internal K(+), Na(+) and sucrose affect the resting and spike potentials similarly. Some organic cations (guanidine, choline, tris, and TMA) behave like sucrose while some other organic cations (TEA, TPA, and TBA) have a specific effect and prolong the spike potential if they are applied intracellularly or extracellularly. In all cases the active membrane potential increases linearly with the logarithm of [Ca(++)](out)/[K(+)](in) and the increment is about 29 mv for tenfold increase in this ratio. The fiber membrane is permeable to Cl(-) and other smaller anions (Br(-) and I(-)) but not to acetate(-) and larger anions (citrate(-), sulfate(-), and methanesulfonate(-)).
Constant current pulses have been applied to single muscle fibers of the barnacle, Balanus nubilus Darwin, with an axial metal electrode. The membrane potential change, which took place over a large part of the muscle fiber, was measured with a similar electrode. Depolarizing pulses, if the voltage was greater than threshold, produced tension. The size of the tension was a function of the magnitude and the duration of the depolarizing pulses. The latency between the onset of depolarization and tension can be only in part attributable to mechanical factors. AC stimulation produced tension, but 5 to 10 seconds were required for the steady-state level of the tension to be reached. Muscles were depolarized in elevated K and studied after the contracture had terminated. If not too depolarized, further depolarization produced tension. Termination of hyperpolarizing pulses also produced tension, which decayed quite slowly. Hyperpolarizing pulses reduced, or abolished, any preexisting tension. Thus, it appears that at certain values of the membrane potential tension is set up, but there is also a slow process of accommodation present.
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