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Their Role in the Causes of Myasthenia Gravis

Donald R. Gentner, PhD; Roger N. Rosenberg, MD

Arch Neurol. 1972;27(6):521-525.

Abstract
Choline acetyltransferase, acetylcholinesterase, and pseudocholinesterase levels were measured in needle biopsy samples of deltoid muscle from subjects with myasthenia gravis and from normal controls. Choline acetyltransferase activities were about 30% lower and acetylcholinesterase activities about 45% lower in myasthenics as compared with controls. These decreased activities, however, are not significant in the cause of the disease; it is postulated that the primary defect at the neuromuscular junction may be the presence of a false transmitter in the synaptic vesicle or defective release of the vesicle contents at the synaptic cleft.

Author Affiliations
La Jolla, Calif

From the departments of neurosciences and pediatrics, and the Division of Neurology, University Hospital, University of California at San Diego, School of Medicine, La Jolla, Calif.

Footnotes
Accepted for publication June 16, 1972.

Reprint requests to Department of Neurosciences, University of California at San Diego, School of Medicine, La Jolla, Calif 92037 (Dr. Rosenberg).

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