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