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Peter Kornfeld, MD; Andrew Somlyo, MD; Kermit E. Osserman, MD

Arch Neurol. 1969;21(5):466-470.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

AT THE present time, all available evidence points to the presynaptic portion of the motor end-plate as the site of defect in myasthenia gravis.^1-4 There appears to be a deficiency in the size of quanta of acetylcholine (ACh) released from a stimulated motor nerve terminal.⁵ With low calcium and high magnesium in extracellular fluid, quantal release of ACh per nerve impulse is small and miniature end-plate potential amplitude is depressed.^5-8 Increasing extracellular level of calcium results in increased release of ACh from presynaptic terminals while magnesium ions act in an opposite direction.^3,9 Del Castillo and Katz¹⁰ and others have shown that while both calcium and magnesium compete for some specific molecule in the presynaptic membrane, only the calcium complex but not the magnesium complex with this molecule could be dissociated by nerve impulse. This activated complex, in turn, would release ACh. Hubbard et al . . . [Full Text PDF of this Article]

Author Affiliations
New York

From the Department of Medicine and Myasthenia Gravis Clinic and Research Laboratory, Mount Sinai School of Medicine, City University of New York, New York.

Footnotes
Submitted for publication April 23, 1969; accepted June 20.

Reprint requests to the Department of Medicine, Mount Sinai School of Medicine, Fifth Ave and 100th St, New York 10029 (Dr. Kornfeld).

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