Opiate peptides, particularly Met-enkephalin, have been shown to block or reduce Ca2+-dependent events in a variety of neurones. Our own observations on the effect of enkephalin on developing Rohon-Beard neurones in Xenopus spinal cord suggested that enkephalin might interact directly with Ca2+ channels in vertebrate neurones. This possibility prompted us to look for an effect of enkephalin on another population of neuronal Ca2+ channels - those in the presynaptic terminals at the frog neuromuscular junction. We were encouraged to try this preparation by an early report that morphine, in rather high concentrations, reduced the amount of acetylcholine (ACh) released from frog muscle by nerve stimulation. Our present results indicate that Met-enkephalin reversibly and specifically reduces the quantal content of transmitter release from nerve terminals in the frog cutaneous pectoris muscle, probably by means of an effect on inward Ca2+ current.
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