Excitation-contraction coupling: role of K-activation within the transverse tubular system.

Abstract

Long-duration Ca action potentials induced in crustacean muscle fibers after prolonged exposure to quaternary ammonium ions are accompanied by attenuated tensions with unique time courses. The tensions have three phases. The initial phase, correlated with the upstroke ofthe spike, is a rapid increase in tension followed by relaxation to or near to resting level (on-ten? sion). In the second phase, tension rises slowly as the spike plateaudeclines. The final phase is another rapid increase and decay in tension that is correlated with termination of the action potential (off-tension). To observe these tensions, fibers must be exposed to 50-100 mM tetrabutylammonium ion for about 1 hr or to lower concentrations for longer periods (e.g., 5 mM for 20-30 hr). To obtain a similar response in fibers treated with tetraethylammonium ion, higher concentrations or longer soaking periods, or both, are required. Because neither caffeine-induced tensions in intact fibers nor contractile protein and sarcoplasmic reticulum function in skinned fibers were modified by quaternary ammonium ions, their site of action appears to be limited to surface or transverse tubular system membranes, or both. The unique tensions can be explained by considering the mode by which quarternary ammonium ions block K channels in conjunction with a scheme in which activation of K channels within the transverse tubular system controls the driving force for influx of Ca ions.The function of the transverse tubular system (TTS) in excitation-contraction coupling (ECC) is to convey a signal to the contractile units throughout the cross section of muscle fibers (1, 2). The characteristics ofthis signal are determined, in part, by the membrane ionic conductances and changes in conductance toward specific ions. For example, in frog muscle a regenerative increase in Na conductance ofthe tubular membrane causes the spread of depolarization throughout the TTS (3, 4).In crustacean fibers Ca activation leads to an influx of Ca ions across the tubular membrane (5), which has been suggested to be the excitatory signal (6-8) or to serve to deliver sufficient quantities of Ca ions for activation of the contractile proteins (9). Other studies on frog and crustacean fibers raised questions regarding the participation of an inward Cl current (Icl) (6,10) and an outward K current (IK) (11,12) in the signaling process. Data gathered to test the possible involvement ofCl in the ECC are inconclusive (6), and a direct role of K activation in signaling in frog muscle has been dismissed, based on the lack of a correlation between changes in thresholds for mechanical activation and delayed K rectification (13).We (18).The present data show that tensions accompanying long-duration Ca spikes elicited in fibers exposed to R4N ions for extended times are not only attenuated (14, 15), but follow a unique time course. These data can be explained by considering the above described interaction of R4N ions with K channels, ifan increase in K conductance and outward IK are integr...

Permeability changes induced by L‐glutamate at the crayfish neuromuscular junction.

“…The refractory period for caffeine contractures in TBA-treated fibres was unaffected by electrical stimulation and appeared to be inifinite. The mechanism by which TBA blocks contraction will be discussed further in another paper (Reuben, Katz, Brandt, Suarez-Kurtz & Dekin, 1982). …”

Excitation–contraction coupling in crab muscle fibers with swollen T tubules

“…External Ba ions and intracellular TBA (after diffusion across the sarcolemma; cf. Reuben et al, 1983) block K currents through the delayed rectifier or voltage-dependent channels (IK,V ;Weman and Gmndfest, 1961 ;Keuken et al, 1983). Thus.…”