The effect of opiates on the terminal nerve impulse and quantal secretion from visualized amphibian nerve terminals

1 Secretion of transmitter from amphibian motor nerve terminal release sites is intermittent, spatially non‐uniform and varies considerably throughout the year and during development. The role of opioid receptors in modulating transmitter secretion from amphibian motor nerve terminals is evaluated in this study. 2 Dynorphin‐A (24 μM) and morphine (500 μM) did not significantly change the shape of the nerve impulse or the consistency with which it was observed, but decreased evoked quantal secretion by more than 50%. These effects of dynorphin‐A and morphine were largely reversed by naloxone (50 μM). 3 Dynorphin‐A and morphine did not significantly change either the amplitude or the frequency of spontaneous quantal secretions. 4 There was a uniform decrease in evoked quantal secretion from release sites along terminal branches, irrespective of the quantal content value before drug treatment, indicating no difference in the susceptibility of proximal vs distal release sites to opiates. 5 Increasing the extracellular calcium concentration (0.3 to 0.4 mM) or trains of conditioning‐test impulses (25 to 100 Hz) resulted in smaller dynorphin‐A or morphine‐induced decreases in evoked quantal secretion. 6 The decrease in evoked quantal secretion occurs as a result of a uniform decrease in the probability of quantal secretion from release sites without any affect on the propagation of the nerve terminal impulse. Low probability release sites become effectively silent.