Reduced acetylcholine-induced channel activity in dystrophic mouse myotubes.
Single channel recording patch-clamp technique was used in the mouse to compare the acetylcholine (ACh)-induced channel behaviour between normal and dystrophic myotubes. While open time and slope conductance were equivalent, ACh-induced channel opening frequency was more than 4-fold reduced in dystrophic compared to normal myotubes. In addition, the steady-state phosphorylation of the ACh receptor (AChR), tested by immunoprecipitation of 32P-labeled cells, indicated that the alpha-subunit was more heavily phosphorylated in the dystrophic myotubes. We propose that the degree of alpha-subunit phosphorylation of the AChR, which parallels the reduced AChR-channel opening probability, determines desensitization of the AChR in dystrophic myotubes.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002460:Cell Line; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009132:Muscles / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D009137:Muscular Dystrophy, Animal / Q000378:metabolism / Q000503:physiopathology*; D010766:Phosphorylation; D011950:Receptors, Cholinergic / Q000378:metabolism* / Q000502:physiology
D007473:Ion Channels; D011950:Receptors, Cholinergic; D000109:Acetylcholine