Trauma-induced changes of skeletal muscle membrane: decreased K+ and increased Na+ permeability

Trauma of skeletal muscle causes membrane depolarization and reduces membrane resistance. The underlying mechanisms were studied in isolated mouse phrenic nerve diaphragms subject to sharp transections of muscle. Depolarization was most marked at the vicinity (similar to 1 mm) of trauma, where the membrane potential dropped rapidly from about -80 mV to zero and repolarized to about -25 mV. At the end-plate region (located similar to 3 mm away from the cut end), the membrane gradually attained a plateau potential around -45 mV. The magnitude of depolarization was not reduced by inhibition of Na+, Ca2+, or Cl- channel, whereas the progress of depolarization was delayed in low-Na+ medium. Activation of the K+ channel with lemakalim induced some hyperpolarization at damaged site but produced a glybenclamide-sensitive outward current and hyperpolarization of end-plate region to the levels before trauma, as if there was no diminution of transmembrane K+ gradient in this area. Appropriate elevation of extracellular K+ to stimulate K+ conductance also hyperpolarized the end-plate region. The results suggest that depolarization at regions remote from trauma is related to decreased K+ and increased Na+ permeability. The cytoplasma compartmentalization and permeability changes may protect muscle fiber from trauma.