Physiological basis of a steady endogenous current in rat lumbrical muscle

J Gen Physiol. 1984 Feb;83(2):175-92. doi: 10.1085/jgp.83.2.175.


In an attempt to determine the mechanism by which rat skeletal muscle endplates generate a steady outward current, we measured the effects of several drugs (furosemide, bumetanide, 9-anthracene carboxylic acid [9-AC]) and changes in external ion concentration (Na+, K+, Cl-, Ba++) on resting membrane potential (Vm) and on the steady outward current. Each of the following treatments caused a 10-15-mV hyperpolarization of the membrane: replacement of extracellular Cl- with isethionate, addition of furosemide or bumetanide, and addition of 9-AC. These results suggest that Cl- is actively accumulated by the muscle fibers and that the equilibrium potential of Cl- is more positive than the membrane potential. Removal of external Na+ also caused a large hyperpolarization and is consistent with evidence in other tissues that active Cl- accumulation requires external Na+. The same treatments greatly reduced or abolished the steady outward current, with a time course that paralleled the changes in Vm. These results cannot be explained by a model in which the steady outward current is assumed to arise as a result of a nonuniform distribution of Na+ conductance, but they are consistent with models in which the steady current is produced by a nonuniform distribution of GCl or GK. Other treatments (Na+-free and K+-free solutions, and 50 microM BaCl2) caused a temporary reversal of the steady current. Parallel measurements of Vm suggested that in none of these cases did the electrochemical driving force for K+ change sign, which makes it unlikely that the steady current arises as a result of a nonuniform distribution of GK. All of the results, however, are consistent with a model in which the steady outward current arises as a result of a nonuniform distribution of Cl- conductance, with GCl lower near the endplate than in extrajunctional regions.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Anthracenes / pharmacology
  • Axons / metabolism
  • Barium / pharmacology
  • Biological Transport, Active / drug effects
  • Bumetanide / pharmacology
  • Cell Membrane / metabolism
  • Chlorides / metabolism*
  • Decapodiformes
  • Furosemide / pharmacology
  • Ion Channels / drug effects
  • Ion Channels / metabolism*
  • Membrane Potentials / drug effects
  • Models, Biological
  • Motor Endplate / metabolism
  • Muscles / metabolism*
  • Rats


  • Anthracenes
  • Chlorides
  • Ion Channels
  • Bumetanide
  • Barium
  • 9-anthroic acid
  • Furosemide