Abstract
Polymerization of filamentous (F)-actin at the neuronal synapse plays an important role in neuronal function. However, the regulatory mechanisms controlling the levels of synaptic actin remain incompletely understood. Here, I used established pharmacological blockers to acutely disrupt the function of actin polymerization machinery, then quantified their effect on synaptic F-actin levels. Synaptic F-actin was modestly decreased by inhibition of Arp2/3-dependent actin branching. Blockade of formin-dependent actin elongation resulted in an Arp2/3-dependent increase in synaptic actin that could be mimicked by limited actin depolymerization. Limited actin depolymerization was also sufficient to reverse a decrease in synaptic F-actin caused by prolonged blockade of synaptic NMDA-type glutamate receptors. These results suggest that interplay between different actin polymerization pathways may regulate synaptic actin dynamics.
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