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The Uptake of 3H(G)L Leucine into Single Muscle Fibers in Charcot-Marie-Tooth Disease

Published online by Cambridge University Press:  18 September 2015

George Monckton  and
Halyna Marusyk
George Monckton*
Affiliation:
Muttart-Collip Memorial Electron Microscope Laboratory, Division of Neurology, Department of Medicine, University of Alberta
Halyna Marusyk
Affiliation:
Muttart-Collip Memorial Electron Microscope Laboratory, Division of Neurology, Department of Medicine, University of Alberta
*
9-101 Clinical Sciences Bldg., University of Alberta, Edmonton, Alberta, Canada T6G 2G3.
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In previous studies, the incorporation of 3H(G)L-leucine into muscles of patients with Charcot-Marie-Tooth (CMT) disease was shown to he increased in comparison with that observed in motor neuron disease (MND). To determine the cause of the increased uptake in CMT, studies of single fiber leucine incorporation have been undertaken. The results of this study indicate that the increased incorporation is into those muscle fibers which are undergoing regeneration following reinnervation. These results do not support the thesis that there is an associated myopathic process in CMT.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 5 , Issue 2 , May 1978 , pp. 199 - 204
Copyright
Copyright © Canadian Neurological Sciences Federation 1978

References

REFERENCES

Coers, C. (1970). Changes in motor unit pattern in the Charcot-Marie-Tooth peroneal muscular atrophy as compared to spinal muscular atrophy. In press, IV Journees Internationales De Pathologie Neuro-Musculaire.Google Scholar
Engel, W.K. (1976b). Muscle biposies in neuromuscular diseases. Pediatr Clin Am, 24, 963–995.Google Scholar
Goldberg, A.L. (1969). Effects of denervation and cortisone on protein catabolism in skeletal muscle. J. Biol. Chem., 244, 3223–3229.CrossRefGoogle ScholarPubMed
Haase, G.R. and Shy, G.M. (1960). Pathological changes in muscle biopsies from patients with peroneal muscular atrophy. Brain, 83, 631–637.CrossRefGoogle ScholarPubMed
Korneliussen, H. (1972). Identification of muscle fiber types in “semithin” sections stained with p-phenylenediamine. Histochemie, 32, 95–98.CrossRefGoogle Scholar
Monckton, G. and Marusyk, H. (1977). An autoradiographic study of muscular dystrophy, motor neuron disease and Charcot-Marie-Tooth disease. Can. J. Neurol. Sci., 4, 25–29.CrossRefGoogle ScholarPubMed
Mumenthaler, M. (1970). Myopathy in neuropathy. In “Muscle Diseases”. Excerpta Medica Amsterdam, Ed. Walton, J.N., Canal, L., and Scarlato, G. pp. 585–598.Google Scholar
Rogers, A.W. (1969). Techniques of autoradiography. New York, Elsevier Publishing Co.Google Scholar
Sissons, H.A. (1963). Investigations in muscle fiber size in: Research in Muscular Dystrophy (Ed.: by members of Research Committee, Muscular Dystrophy Group). Pittman Medical, London.Google Scholar
TomÉ, F.M.S. and Fardeau, M. (1976). Muscle and nerve biopsies studies in Charcot-Marie-Tooth disease. In press, IV Journées Internationales De Pathologie Neuro-Musculaire.Google Scholar
Wohlfart, G. (1957). Nerve regeneration in amyotrophic lateral sclerosis. Neurology, 7, 124–134.CrossRefGoogle ScholarPubMed