The Role of Calcium in Triggering the Release of Transmitter at the Vertebrate Neuromuscular Junction. An Analysis of the Effects of Drugs
Katz (1) in his Sherrington lecture summarized our understanding of the microphysiology of the presynaptic terminals of the vertebrate neuromuscular junction (nmj). The arrival of a nervous impulse causes a transient increase in the calcium permeability of the plasma membrane and the associated entry of calcium ions triggers the synchronized release of quanta of transmitter. The magnitude of the evoked response, recorded as the endplate potential (EPP) is therefore primarily dependent on the concentration of extracellular calcium (2). There is also a spontaneous release of quantal packets of acetylcholine (ACh), recorded as the miniature endplate potentials (MEPPs), and the MEPP frequency is determined, at least in part, on the other hand, by the concentration of intracellular calcium at the terminals (3, 4). However, we still lack a firm conclusion as to how the intracellular calciumions trigger both the spontaneous and the evoked release of transmitter. Since the earlier biophysical studies of Katz and Miledl a large number of pharmacological agents have been tested on the vertebrate nmj, and the purpose of this very brief review is to attempt to determine their sites of action in the hope of discovering some of the biochemical events of exocytosis.
KeywordsBotulinum Toxin Neuromuscular Junction Transmitter Release Spontaneous Release Presynaptic Nerve Terminal
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