Effects of Veratrine, Nitrate Ion and γ-Aminobutyric Acid on Mammalian Miniature End-Plate Potentials

Abstract

DAHLBÄCK et al.¹ have found that the frequency with which miniature end-plate potentials appear at the neuromuscular junctions is significantly reduced in myasthenia gravis. Since these potentials are assumed to represent the spontaneous release of transmitter substance from motor nerve endings the defect in myasthenia has been considered to be of presynaptic origin. However, agents which help the clinical disorder do not greatly affect the frequency of miniature end-plate potentials, and for this reason it is still necessary to consider possible alternative mechanisms which may operate independently of, or in conjunction with, the defect in the presynaptic release. One possibility is that the transmitter ‘quanta’ fail to cross the synapse because of morphological abnormalities in the latter². Equally, the end-plate may be resistant to the transmitter substance. Thus a decrease in the frequency of miniature depolarizations might reflect a degree of failure in transmitter diffusion or indicate an abnormality in the responsiveness of the membrane to ionic influx. The first possibility cannot easily be tested, but the second can conveniently be studied by recording the frequencies and amplitudes of post-synaptic events under various test conditions.