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A freeze‐fracture analysis of intramembrane particle densities on dystrophic hamster heart sarcolemma
Author(s) -
Graham Kathryn A.,
Shivers Richard R.,
Atkinson Burr G.
Publication year - 1984
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880070702
Subject(s) - sarcolemma , hamster , muscular dystrophy , myocyte , cardiac muscle , skeletal muscle , biology , dysferlin , population , mesocricetus , anatomy , medicine , endocrinology , genetics , environmental health
The intramembrane particle (IMP) profile of control and dystrophic (Bio 14.6) hamster cardiac muscle plasma membrane was assessed in freeze‐fracture replicas to determine whether this animal model of muscular dystrophy exhibits the same membrane characteristics found in skeletal muscle from other more thoroughly studied dystrophic animals, and to test the hypothesis that the plasma membrane of the cardiac muscle cell is the site of a defect associated with the disease. Samples of cardiac muscle tissue from hamsters ranging in age from 1 to 13 months were freeze‐fractured. Intramembrane particle numbers were determined for all tissue samples by counting randomly selected areas of Phyphen; and E‐face surfaces. Up to the age of 1 month, the particle density was the same in both strains of hamster, after which time, the population of IMPs was about 30% lower in dystrophic than in normal heart sarcolemma. This 30% difference in particle frequency in dystrophic hamster heart membrane is consistent with values published for cell membrane from other muscular dystrophies and supports the theory that there is a defect in the plasma membrane of dystrophic cells. In addition, this study has shown for the first time that a presumed membrane defect related to muscular dystrophy (reduced number of IMPs) may be present throughout the life of the animal (1–13 months), and expressed in every cell sampled.