Parallels between spontaneous release of transmitter at the neuromuscular junction and subcellular damage of muscle. Evidence for the underlying common involvement of intracellular Ca 2+?

Abstract

1. 1. Parallels between the rate of spontaneous release of transmitter at the neuromuscular junction and the triggering of ultrastructural damage in cardiac and skeletal muscle cells are reviewed. 2. 2. Agents that increase release at the presynaptic terminals promote damage; treatments that may protect muscle cells also suppress transmitter release. 3. 3. It is suggested that changes in [Ca 2+] i are involved in both tissues and the possible implications for dystrophic muscle are discussed.