Stretch‐sensitive channels in developing muscle cells from a mouse cell line.

Abstract

4. Channel openings occurred as bursts of brief openings and closings separated by much longer closed periods. Closed-time histograms were best fitted with three exponential components, while histograms of burst duration were best fitted with two exponential components, reflecting the short and long bursts in the single-channel records.5. Applying suction to the patch electrode while recording at steady negative membrane potentials produced channel openings to discrete current levels. Mean channel open probability depended linearly on the square of the applied pressure and was greater at positive membrane potentials. The permeability of the channel to monovalent and divalent cations was indistinguishable from the spontaneous activity recorded at steady negative potentials.6. Channel activity recorded from cell-attached patches in the absence of applied pressure depended on membrane potential increasing -e-fold per 38 mV with depolarization. Analysis of the kinetics of the response to membrane potential * To whom correspondence should be addressed. MS 7995A. FRANCO AND J. B. LANSMAN showed that the depolarization reduced the duration of the slowest component of the closed-time distribution.7. The lanthanide cation gadolinium (Gd) reduced the amplitude of the unitary currents in a concentration-dependent manner. The amplitudes of both inward and outward currents were reduced to the same extent suggesting block is voltageindependent. Gd produced half-maximal inhibition of the unitary current at 6 aM.8. The fraction of recordings from cell-attached patches showing stretch-activated and spontaneous channel activity was determined at morphologically identifiable stages of myogenesis. Stretch-sensitive activity was high in myoblasts plated at low density, but decreased during development. The fraction of patches showing spontaneous activity was low and remained constant during muscle differentiation.9. The results are discussed in terms of the possibility that cation channels in developing muscle cells are gated by changes in membrane tension and voltage. The role of Ca2+-permeable cation channels in providing a pathway for Ca2+ influx during the early stages of myogenesis is considered.

Regulation of TRPC1 and TRPC4 Cation Channels Requires an α1-Syntrophin-dependent Complex in Skeletal Mouse Myotubes

“…Moreover, stretch-activated currents share similar electrophysiological properties with store-operated currents when recorded at the surface membrane of skeletal fibers (23). Stretch-activated currents (27,60) and osmotic activated calcium entry (33) are increased in mdx and DMD muscle cells lacking dystrophin and DAPC. It is thus possible that the loss of the PDZ-mediated regulation by ␣1-syntrophin in dystrophin-deficient muscles enhances the mechanical sensitivity of TRPC1-containing channels.…”

Maturation and myotonia influence the abundance of cation channels K DR , K IR and C IR differently: a patch-clamp study on mouse interosseus muscle fibres

“…Systematic application of pressure was not possible with our recording equipment, but there was no indication of sensitivity to membrane deformation. Furthermore, whereas C IR rectifies inwardly, the mechanosensitive channels show outwards currents with a high open probability [10]. Low abundance in adult muscle, low open probability and rundown upon patch excision may explain why C IR has not been recorded in previous studies on native mammalian muscle fibres [4,8,16].…”

Enhanced activity of eccentric contraction induces alterations in <i>in vitro</i> sarcoplasmic reticulum Ca²⁺ handling in rat hindlimb muscles

“…Elevated [Ca 2+ ]f is, in turn, crucial to a mechanism that further increases Ca 2+ concentration. The [Ca 2+ ]f elevation could activate stretch-sensitive nonspecific cation channels that exist in sarcolemma and pass Ca 2+ and K+ into the cytoplasm 5,6) . Alternatively, [Ca 2+ ]f elevation could initiate impairment of excitation-contraction coupling by activating various proteolytic and degradative pathways 30) as well as promoting Ca 2+ inflow into the cytosol.…”

“…ECC leads to increases in the intracellular free Ca 2+ concentration ([Ca 2+ ]f) as a consequence of the opening of a stretch-sensitive, nonspecific cation channel 5,6) , and/or protein degradation that is induced by repeated mechanical overstretching of sarcomeres 4) might contribute to the decline of the contractile force. Because the regulation of [Ca 2+ ]f is primarily accomplished by SR in skeletal muscle, it has been proposed that dysfunctions of SR in skeletal muscle may cause the loss of force that occurs as a result of eccentric exercise 7) .…”

“…Previous studies showed that Na + -K + -ATPase activity was reduced with heavy isometric 15) , isokinetic 16) , and progressive exercise 17) . ECC might elicit the formation of abnormal membranes that are involved in the excitation-contraction coupling process 18) and the pronounced increases in intracellular Na + concentration ([Na + ]i) 19) by Na + entry through ECC-induced fiber muscle membrane disruption and t-tubule tears 5) or the opening of stretch-sensitive cation channels 5,6) . However, few studies have focused on ECC-induced alterations in Na + -K + -ATPase.…”