Departmental Papers (ASC)

Document Type

Technical Report

Date of this Version

10-2005

Publication Source

Journal of Neuroscience

Volume

25

Issue

43

Start Page

9949

Last Page

9959

DOI

10.1523/JNEUROSCI.3169-05.2005

Abstract

In the CNS, receptor recycling is critical for synaptic plasticity; however, the recycling of receptors has never been observed at peripheral synapses. Using a novel imaging technique, we show here that nicotinic acetylcholine receptors (AChRs) recycle into the postsynaptic membrane of the neuromuscular junction. By sequentially labeling AChRs with biotin-bungarotoxin and streptavidin-fluorophore conjugates, we were able to distinguish recycled, preexisting, and new receptor pools at synapses in living mice. Time-lapse imaging revealed that recycled AChRs were incorporated into the synapse within hours of initial labeling, and their numbers increased with time. At fully functional synapses, AChR recycling was robust and comparable in magnitude with the insertion of newly synthesized receptors, whereas chronic synaptic activity blockade nearly abolished receptor recycling. Finally, using the same sequential labeling method, we found that acetylcholinesterase, another synaptic component, does not recycle. These results identify an activity-dependent AChR-recycling mechanism that enables the regulation of receptor density, which could lead to rapid alterations in synaptic efficacy.

Copyright/Permission Statement

This article is distributed Open Access under a Creative Commons Attribution 4.0 International license (https://creativecommons.org/licenses/by/4.0/).

Keywords

toxin, turnover, synaptic transmission, neuromuscular junction, trafficking, acetylcholine receptor (AChR)

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Date Posted: 15 June 2018

This document has been peer reviewed.