Depolymerization of actin by latrunculin A transiently promotes neurotransm
itter release. The mean rate of mEPSCs increases by a Ca2+-independent proc
ess, without a concomitant change in the mean amplitude. The readily releas
able vesicle pool size and the rate of refilling of the readily releasable
pool remain unaltered by latrunculin treatment. Evoked neurotransmitter rel
ease also increases in a manner consistent with an increase in vesicle rele
ase probability. The observed enhancement of neurotransmitter release is sp
ecific to actin depolymerization mediated by latrunculin A and is not cause
d by cytochalasin D. Our findings indicate that actin participates in a reg
ulatory mechanism that restrains fusion of synaptic vesicles at the active
zone.