A freeze-fracture study of normal and dystrophic C57BL mouse muscle.
Freeze-fracture replicas of normal and dystrophic C57BL mouse muscle and kidney were examined to see whether here was a deficit in plasmalemmal particles which others suggest is a feature of dystrophies. When compared with normal membranes there was an increase in the particle density in dystrophic extensor digitorum longus muscle, a decrease in dystrophic soleus muscle, and no change in dystrophic kidney. Therefore there was not a general deficit in intramembrane particles in this dystrophic tissue. Indirect evidence supported the hypothesis that abnormalities in dystrophic mouse muscles are caused by abnormal motor input. The density of indentations, parallel to the T-tubule, on the flat surface of the terminal cisternae can be modulated by the motor nerve. Changes were found in indentation density in dystrophic muscle which were similar to changes seen after transection of the spinal cord in the mid-thoracic region. There were parallel changes in contractile properties and indentation density in dystrophic fibers.
D000818:Animals; D002462:Cell Membrane / Q000648:ultrastructure; D005614:Freeze Fracturing; D007668:Kidney / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D009132:Muscles / Q000473:pathology; D009137:Muscular Dystrophy, Animal / Q000473:pathology*; D012519:Sarcoplasmic Reticulum / Q000648:ultrastructure