Cycling of actin assembly in synaptosomes and neurotransmitter release

Neuron. 1989 Aug;3(2):257-65. doi: 10.1016/0896-6273(89)90039-1.


We have investigated the regulation of actin assembly in whole mouse brain synaptosomes and how that regulation modulates neurotransmitter release. During a 30 s depolarization with high K+, filamentous actin (F-actin) levels, monitored by staining with rhodamine phalloidin, increase dramatically (up to 300% in 3 s), decrease, and increase once again. This F-actin cycling is regulated by pathways both dependent and independent of Ca2+ influx and is markedly affected by exposing synaptosomes to Li+, tetrodotoxin, and diacylglycerol. Measurement of [3H]norepinephrine release from synaptosomes containing entrapped agents that modulate actin assembly (DNAase I or phalloidin) indicates that actin depolymerization is necessary for normal release and that repolymerization limits release.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Actins / metabolism*
  • Animals
  • Membrane Potentials / physiology
  • Mice
  • Nerve Endings / metabolism
  • Nerve Endings / physiology
  • Nerve Endings / ultrastructure
  • Neurotransmitter Agents / metabolism*
  • Neurotransmitter Agents / physiology
  • Norepinephrine / metabolism
  • Synaptosomes / metabolism*
  • Synaptosomes / physiology
  • Synaptosomes / ultrastructure


  • Actins
  • Neurotransmitter Agents
  • Norepinephrine