Ionic currents in slow twitch skeletal muscle in the rat.

Abstract

SUMMARY1. The ionic currents in slow fibres isolated from rat soleus muscle have been studied under voltage-clamp conditions with a double sucrose-gap method and the results are compared to those obtained from fast fibres isolated from the iliacus muscle.2. The mean value of the resting potential in slow fibres is -70 mV, a value 8 mV more positive that the mean resting potential of fast fibres (-78 mV).3. In slow muscle, a fast inward current which is blocked by tetrodotoxin and which depends on external sodium concentration is presumed to be carried by sodium ions. The characteristics of this current, which are time-and voltagedependent, are similar to those of the iliacus fibres. From a holding potential at -86 mV, this inward current is maximal (2-6 mA/cm2 + 0.3) at + 491 mV + 1.5 (mean + S.E. of mean), reverses at + 127-3 mV + 2-2 (mean+ S.E. of mean), and its half inactivation occurs at + 23-2 mV + 0-8 (mean + s.E. of mean).4. The delayed outward current in slow fibres is unchanged by exposure to chloride free solution and has a time course very different from that found in fast fibres. This current reaches an initial peak in 5-10 msec and a second peak or steady level after 40-150 msec. The decay of the outward current is also very different, being ten times slower than that in fast fibres (1500-3000 msec).5. Analysis of the tail currents reveals the existence of two components of delayed current in slow fibres. The faster component reverses at a potential of 113 mV + 0 9 (mean + s.E. of mean) positive to the holding potential (equivalent to a membrane potential of about -75 mV), in contrast to a reversal potential of 35.4 mV + 2-5 (mean + S.E. of mean) positive to the holding potential for the slower component (equivalent to a membrane potential of about -51 mV.6. In L-glutamate solution the characteristics of the inward-going rectification are the same in the two types of muscle.

Na+ current densities and voltage dependence in human intercostal muscle fibres.

“…In rat and rabbit skeletal musle, fibres from predominantly fast-twitch muscles had more negative values for Vi,Namax' h,2 VI' and resting membrane potential, larger INamax on extrajunctional membrane, and smaller values for Ah and A. compared to fibres from predominantly slow-twitch muscles (Duval & Leoty, 1980;Kirsch & Anderson, 1986;Ruff et al 1987;Simoncini & Stiihmer, 1987). Recent work suggests that rat fast-twitch muscle fibres have higher densities of Na+ channels on the endplate border and extrajunctional membrane compared to slow-twitch fibres and that fasttwitch fibres show a greater increase in Na+ channel density near the endplate than is true for slow-twitch fibres (Ruff, 1991;R.…”

Inward rectifier potassium currents in mammalian skeletal muscle fibres

“…). In contrast, IKir measurements in mammalian skeletal muscle fibres are scarce (Duval & Leoty, ; Beam & Donaldson, ; Barrett‐Jolley et al . ) and have yielded an incomplete characterization of the functional properties of Kir channels in their natural environment.…”

“…The properties of Kir currents (IKir) were extensively investigated in amphibian muscle fibres (Hodgkin & Horowicz, 1959b, 1960Standen & Stanfield, 1978b;Leech & Stanfield, 1981;Stanfield et al 2002) where they have been shown to originate at the surface and transverse tubular system (TTS) membranes (Almers, 1972b;Standen & Stanfield, 1979;Ashcroft et al 1985). In contrast, IKir measurements in mammalian skeletal muscle fibres are scarce (Duval & Leoty, 1980;Beam & Donaldson, 1983;Barrett-Jolley et al 1999) and have yielded an incomplete characterization of the functional properties of Kir channels in their natural environment.…”

Structural Insights into GIRK Channel Function

“…Surprisingly, the gating of inward current shifted with different extracellular K + concentrations, instead of occurring over a fixed range of membrane potentials (Katz, 1949). This "anomalous rectification," subsequently referred to as inward rectification, was later observed in a wide variety of tissues including brain (Andrade, Malenka, & Nicoll, 1986;Andrade & Nicoll, 1987;Inoue, Nakajima, & Nakajima, 1988;North, Williams, Surprenant, & Christie, 1987;Penington, Kelly, & Fox, 1993), heart (Breitwieser & Szabo, 1985;Kurachi, 1985;Pfaffinger, Martin, Hunter, Nathanson, & Hille, 1985;Vereecke, Isenberg, & Carmeliet, 1980), skeletal muscle (Barrett-Jolley, Dart, & Standen, 1999;Beam & Donaldson, 1983;Duval & Leoty, 1980;Stanfield, Nakajima, & Nakajima, 2002), kidney (Hebert, 1995;Ho et al, 1993), and pancreas (Cook & Hales, 1984;Findlay, Dunne, & Petersen, 1985;Isomoto et al, 1996;Iwanir & Reuveny, 2008;Yoshimoto et al, 1999), in addition to blood cells (Lewis, Ikeda, Aryee, & Joho, 1991;McKinney & Gallin, 1988) and oocytes (Hagiwara, Miyazaki, & Rosenthal, 1976;Hagiwara & Takahashi, 1974). In general, inwardly rectifying K + channels are critical in maintaining the resting membrane potential because the voltage range over which the channel passes outward current is near the cell's resting membrane potential (V m ) (Armstrong & Binstock, 1965;Noble & Tsien, 1968).…”