TY - JOUR
T1 - Abnormal distribution of skeletal muscle acetylcholinesterase molecular forms in dystrophic mice
AU - Skau, K. A.
AU - Brimijoin, S.
N1 - Funding Information:
Abbreviations: AChE-acetylcholinesterase, EDL-extensor digitorum longus. ’ This work was supported in part by National Institutes of Health grant NSI 1855 and Center Grant NS14304. Dr. Brimijoin is a recipient of Research Career Development Award NSOOI 19. Dr. Skau is a recipient of NIH Postdoctoral Fellowship NS06010; his current address is the Department of Biochemical Pharmacology and Toxicology, College of Pharmacy, University of Utah, Salt Lake City, Utah 84112.
PY - 1981/10
Y1 - 1981/10
N2 - Acetylcholinesterase (AChE) activities and molecular forms, as separated by density gradient centrifugation, were studied in dystrophic and clinically normal mouse muscle. Dystrophic hemidiaphragms exhibited normal AChE activity, but there was little or no 10 S enzyme, a form that constitutes 27% of control tissue AChE. The 10 S-AChE abnormality was similarly present in dystrophic extensor digitorum longus (EDL) muscle, but this muscle exhibited significantly reduced AChE activity. The EDL muscles also had reduced 16 S-AChE but normal 4 S enzyme activity. Chronic denervation of EDL muscles resulted in proportionally similar reductions of weight, total AChE, and 16 S enzyme in dystrophic and control muscles. We conclude that murine dystrophy involves some alterations that resemble denervation, but that there are major qualitative and quantitative differences in AChE that cannot be explained by a denervation-like effect.
AB - Acetylcholinesterase (AChE) activities and molecular forms, as separated by density gradient centrifugation, were studied in dystrophic and clinically normal mouse muscle. Dystrophic hemidiaphragms exhibited normal AChE activity, but there was little or no 10 S enzyme, a form that constitutes 27% of control tissue AChE. The 10 S-AChE abnormality was similarly present in dystrophic extensor digitorum longus (EDL) muscle, but this muscle exhibited significantly reduced AChE activity. The EDL muscles also had reduced 16 S-AChE but normal 4 S enzyme activity. Chronic denervation of EDL muscles resulted in proportionally similar reductions of weight, total AChE, and 16 S enzyme in dystrophic and control muscles. We conclude that murine dystrophy involves some alterations that resemble denervation, but that there are major qualitative and quantitative differences in AChE that cannot be explained by a denervation-like effect.
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U2 - 10.1016/0014-4886(81)90152-7
DO - 10.1016/0014-4886(81)90152-7
M3 - Article
C2 - 7286112
AN - SCOPUS:0019517443
SN - 0014-4886
VL - 74
SP - 111
EP - 121
JO - Experimental Neurology
JF - Experimental Neurology
IS - 1
ER -