Control of synaptic vesicle endocytosis by an extracellular signalling molecule

Signalling cascades control multiple aspects of presynaptic function. Synaptic vesicle endocytosis was assumed to be exempt from modulation, due to its essential role maintaining synaptic vesicle supply and thus neurotransmission. Here we show that brain-derived neurotrophic factor arrests the repho...

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Main Authors: Smillie, Karen J., Pawson, Jonathan, Perkins, Emma M., Jackson, Mandy, Cousin, Michael A.
Format: Online
Language:English
Published: Nature Pub. Group 2013
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3778765/
id pubmed-3778765
recordtype oai_dc
spelling pubmed-37787652013-09-23 Control of synaptic vesicle endocytosis by an extracellular signalling molecule Smillie, Karen J. Pawson, Jonathan Perkins, Emma M. Jackson, Mandy Cousin, Michael A. Article Signalling cascades control multiple aspects of presynaptic function. Synaptic vesicle endocytosis was assumed to be exempt from modulation, due to its essential role maintaining synaptic vesicle supply and thus neurotransmission. Here we show that brain-derived neurotrophic factor arrests the rephosphorylation of the endocytosis enzyme dynamin I via an inhibition of glycogen synthase kinase 3. This event results in a selective inhibition of activity-dependent bulk endocytosis during high-intensity firing. Furthermore, the continued presence of brain-derived neurotrophic factor alleviates the rundown of neurotransmission during high activity. Thus, synaptic strength can be modulated by extracellular signalling molecules via a direct inhibition of a synaptic vesicle endocytosis mode. Nature Pub. Group 2013-09-03 /pmc/articles/PMC3778765/ /pubmed/23999152 http://dx.doi.org/10.1038/ncomms3394 Text en Copyright © 2013, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. http://creativecommons.org/licenses/by-nc-nd/3.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Smillie, Karen J.
Pawson, Jonathan
Perkins, Emma M.
Jackson, Mandy
Cousin, Michael A.
spellingShingle Smillie, Karen J.
Pawson, Jonathan
Perkins, Emma M.
Jackson, Mandy
Cousin, Michael A.
Control of synaptic vesicle endocytosis by an extracellular signalling molecule
author_facet Smillie, Karen J.
Pawson, Jonathan
Perkins, Emma M.
Jackson, Mandy
Cousin, Michael A.
author_sort Smillie, Karen J.
title Control of synaptic vesicle endocytosis by an extracellular signalling molecule
title_short Control of synaptic vesicle endocytosis by an extracellular signalling molecule
title_full Control of synaptic vesicle endocytosis by an extracellular signalling molecule
title_fullStr Control of synaptic vesicle endocytosis by an extracellular signalling molecule
title_full_unstemmed Control of synaptic vesicle endocytosis by an extracellular signalling molecule
title_sort control of synaptic vesicle endocytosis by an extracellular signalling molecule
description Signalling cascades control multiple aspects of presynaptic function. Synaptic vesicle endocytosis was assumed to be exempt from modulation, due to its essential role maintaining synaptic vesicle supply and thus neurotransmission. Here we show that brain-derived neurotrophic factor arrests the rephosphorylation of the endocytosis enzyme dynamin I via an inhibition of glycogen synthase kinase 3. This event results in a selective inhibition of activity-dependent bulk endocytosis during high-intensity firing. Furthermore, the continued presence of brain-derived neurotrophic factor alleviates the rundown of neurotransmission during high activity. Thus, synaptic strength can be modulated by extracellular signalling molecules via a direct inhibition of a synaptic vesicle endocytosis mode.
publisher Nature Pub. Group
publishDate 2013
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3778765/
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