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Synaptic vesicle traffic is supported by transient actin filaments and regulated by PKA and NO
Synaptic vesicle traffic is supported by transient actin filaments and regulated by PKA and NO
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Synaptic vesicle traffic is supported by transient actin filaments and regulated by PKA and NO
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Synaptic vesicle traffic is supported by transient actin filaments and regulated by PKA and NO
Synaptic vesicle traffic is supported by transient actin filaments and regulated by PKA and NO
Journal Article

Synaptic vesicle traffic is supported by transient actin filaments and regulated by PKA and NO

2020
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Overview
Synaptic vesicles (SVs) can be pooled across multiple synapses, prompting questions about their dynamic allocation for neurotransmission and plasticity. We find that the axonal traffic of recycling vesicles is not supported by ubiquitous microtubule-based motility but relies on actin instead. Vesicles freed from synaptic clusters undergo ~1 µm bouts of active transport, initiated by nearby elongation of actin filaments. Long distance translocation arises when successive bouts of active transport were linked by periods of free diffusion. The availability of SVs for active transport can be promptly increased by protein kinase A, a key player in neuromodulation. Vesicle motion is in turn impeded by shutting off axonal actin polymerization, mediated by nitric oxide-cyclic GMP signaling leading to inhibition of RhoA. These findings provide a potential framework for coordinating post-and pre-synaptic strength, using retrograde regulation of axonal actin dynamics to mobilize and recruit presynaptic SV resources. Transport of membrane proteins within the cell is thought to mainly rely on microtubule-based transport, but the role of microtubules in neuronal cell recycling of synaptic vesicles is unclear. Here, the authors show that axonal movement of recycling vesicles may be driven not by microtubules but primarily by actin polymerization.