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A surface potential change in the membranes of frog skeletal muscle is associated with excitation‐contraction coupling.
Author(s) -
Jong D S,
Stroffekova K,
Heiny J A
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1997.sp021969
Subject(s) - membrane potential , chemistry , depolarization , voltage sensitive dye , biophysics , surface charge , coupling (piping) , voltage clamp , voltage , membrane , analytical chemistry (journal) , materials science , physics , biochemistry , chromatography , quantum mechanics , metallurgy , biology
1. Voltage changes and intramembrane charge movements in the transverse tubule membranes (T‐system) of frog fast twitch muscle fibres were compared using the potentiometric dye WW‐375 and a Vaseline‐gap voltage clamp. As shown previously, the potentiometric dye reports a dynamic surface potential change that occurs on the myoplasmic face of the T‐system membranes when the macroscopic potential applied across the surface membrane exceeds the mechanical threshold (about ‐60 mV). 2. The voltage dependence of the extra surface potential change and charge movement were found to be similar. Both activated with a sigmoid voltage dependence centred around ‐35 to ‐40 mV, and saturated at voltages above 0 mV. Both processes inactivated upon sustained depolarization, with a mid‐point for inactivation of ‐40 mV. 3. Pharmacological agents which alter charge movement and excitation‐contraction (E‐C) coupling altered the non‐linear surface potential change in a parallel manner. Perchlorate, which potentiates charge movement and E‐C coupling, slowed the activation and deactivation of both charge movement and the non‐linear surface potential change at voltages above ‐40 mV, and shifted the voltage dependence of both processes by 13 14 mV to more negative voltages. Dantrolene, which depresses charge movement and E‐C coupling, shifted the voltage dependence of both processes to more positive voltages. Nifedipine, which suppresses charge movement and E‐C coupling, reduced the magnitude of both charge movement and the non‐linear surface potential change. 4. The non‐linear surface potential change remained after the sarcoplasmic reticulum (SR) was depleted of Ca2+, suggesting that it is not a consequence of Ca2+ release. 5. These results suggest that the non‐linear surface potential change is closely associated with movements of the voltage sensor (dihydropyridine (DHP) receptor) that control E‐C coupling and/or signal transduction across the triadic junction. We propose that the movement of charged intramembrane domains of the DHP receptor which generate charge movement drive a subsequent movement of charged intracellular molecular domains that move within about 1 nm of the T‐system membrane to generate a measurable change in surface charge. For example, the postulated mobile surface charges could be on an intracellular domain of the voltage sensor or closely associated protein, or could be a charged molecular domain of a protein that associates/dissociates with T‐system membrane or DHP receptor during E‐C coupling.