Impaired Recycling of Synaptic Vesicles after Acute Perturbation of the Presynaptic Actin Cytoskeleton

Actin is an abundant component of nerve terminals that has been implicated at multiple steps of the synaptic vesicle cycle, including reversible anchoring, exocytosis, and recycling of synaptic vesicles. In the present study we used the lamprey reticulospinal synapse to examine the role of actin at...

Full description

Saved in:
Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2002-10, Vol.99 (22), p.14476-14481
Main Authors: Shupliakov, Oleg, Bloom, Ona, Gustafsson, Jenny S., Kjaerulff, Ole, Löw, Peter, Tomilin, Nikolay, Pieribone, Vincent A., Greengard, Paul, Brodin, Lennart
Format: Article
Language:English
Subjects:
Actin Cytoskeleton - metabolism
Actins
Actins - metabolism
Animals
Axons
Biological Sciences
Botulinum Toxins - pharmacology
Cell membranes
Cytoskeleton - metabolism
Endocytosis - drug effects
Injection sites
Lampreys
Medicin och hälsovetenskap
Microfilaments
Microinjections
Myosin Subfragments - pharmacology
Neurology
Neurons
Poisons
Presynaptic Terminals - drug effects
Presynaptic Terminals - metabolism
Recycling
Synapses
Synaptic Vesicles - drug effects
Toxins
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Actin is an abundant component of nerve terminals that has been implicated at multiple steps of the synaptic vesicle cycle, including reversible anchoring, exocytosis, and recycling of synaptic vesicles. In the present study we used the lamprey reticulospinal synapse to examine the role of actin at the site of synaptic vesicle recycling, the endocytic zone. Compounds interfering with actin function, including phalloidin, the catalytic subunit of Clostridium botulinum C2 toxin, and N-ethylmaleimide-treated myosin S1 fragments were microinjected into the axon. In unstimulated, phalloidin-injected axons actin filaments formed a thin cytomatrix adjacent to the plasma membrane around the synaptic vesicle cluster. The filaments proliferated after stimulation and extended toward the vesicle cluster. Synaptic vesicles were tethered along the filaments. Injection of N-ethylmaleimide-treated myosin S1 fragments caused accumulation of aggregates of synaptic vesicles between the endocytic zone and the vesicle cluster, suggesting that vesicle transport was inhibited. Phalloidin, as well as C2 toxin, also caused changes in the structure of clathrin-coated pits in stimulated synapses. Our data provide evidence for a critical role of actin in recycling of synaptic vesicles, which seems to involve functions both in endocytosis and in the transport of recycled vesicles to the synaptic vesicle cluster.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.212381799