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Miro1‐dependent mitochondrial positioning drives the rescaling of presynaptic Ca(2+) signals during homeostatic plasticity
Mitochondrial trafficking is influenced by neuronal activity, but it remains unclear how mitochondrial positioning influences neuronal transmission and plasticity. Here, we use live cell imaging with the genetically encoded presynaptically targeted Ca(2+) indicator, SyGCaMP5, to address whether pres...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5286383/ https://www.ncbi.nlm.nih.gov/pubmed/28039205 http://dx.doi.org/10.15252/embr.201642710 |
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author | Vaccaro, Victoria Devine, Michael J Higgs, Nathalie F Kittler, Josef T |
author_facet | Vaccaro, Victoria Devine, Michael J Higgs, Nathalie F Kittler, Josef T |
author_sort | Vaccaro, Victoria |
collection | PubMed |
description | Mitochondrial trafficking is influenced by neuronal activity, but it remains unclear how mitochondrial positioning influences neuronal transmission and plasticity. Here, we use live cell imaging with the genetically encoded presynaptically targeted Ca(2+) indicator, SyGCaMP5, to address whether presynaptic Ca(2+) responses are altered by mitochondria in synaptic terminals. We find that presynaptic Ca(2+) signals, as well as neurotransmitter release, are significantly decreased in terminals containing mitochondria. Moreover, the localisation of mitochondria at presynaptic sites can be altered during long‐term activity changes, dependent on the Ca(2+)‐sensing function of the mitochondrial trafficking protein, Miro1. In addition, we find that Miro1‐mediated activity‐dependent synaptic repositioning of mitochondria allows neurons to homeostatically alter the strength of presynaptic Ca(2+) signals in response to prolonged changes in neuronal activity. Our results support a model in which mitochondria are recruited to presynaptic terminals during periods of raised neuronal activity and are involved in rescaling synaptic signals during homeostatic plasticity. |
format | Online Article Text |
id | pubmed-5286383 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-52863832017-02-03 Miro1‐dependent mitochondrial positioning drives the rescaling of presynaptic Ca(2+) signals during homeostatic plasticity Vaccaro, Victoria Devine, Michael J Higgs, Nathalie F Kittler, Josef T EMBO Rep Scientific Reports Mitochondrial trafficking is influenced by neuronal activity, but it remains unclear how mitochondrial positioning influences neuronal transmission and plasticity. Here, we use live cell imaging with the genetically encoded presynaptically targeted Ca(2+) indicator, SyGCaMP5, to address whether presynaptic Ca(2+) responses are altered by mitochondria in synaptic terminals. We find that presynaptic Ca(2+) signals, as well as neurotransmitter release, are significantly decreased in terminals containing mitochondria. Moreover, the localisation of mitochondria at presynaptic sites can be altered during long‐term activity changes, dependent on the Ca(2+)‐sensing function of the mitochondrial trafficking protein, Miro1. In addition, we find that Miro1‐mediated activity‐dependent synaptic repositioning of mitochondria allows neurons to homeostatically alter the strength of presynaptic Ca(2+) signals in response to prolonged changes in neuronal activity. Our results support a model in which mitochondria are recruited to presynaptic terminals during periods of raised neuronal activity and are involved in rescaling synaptic signals during homeostatic plasticity. John Wiley and Sons Inc. 2016-12-30 2017-02 /pmc/articles/PMC5286383/ /pubmed/28039205 http://dx.doi.org/10.15252/embr.201642710 Text en © 2016 The Authors. Published under the terms of the CC BY 4.0 license This is an open access article under the terms of the Creative Commons Attribution 4.0 (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Scientific Reports Vaccaro, Victoria Devine, Michael J Higgs, Nathalie F Kittler, Josef T Miro1‐dependent mitochondrial positioning drives the rescaling of presynaptic Ca(2+) signals during homeostatic plasticity |
title | Miro1‐dependent mitochondrial positioning drives the rescaling of presynaptic Ca(2+) signals during homeostatic plasticity |
title_full | Miro1‐dependent mitochondrial positioning drives the rescaling of presynaptic Ca(2+) signals during homeostatic plasticity |
title_fullStr | Miro1‐dependent mitochondrial positioning drives the rescaling of presynaptic Ca(2+) signals during homeostatic plasticity |
title_full_unstemmed | Miro1‐dependent mitochondrial positioning drives the rescaling of presynaptic Ca(2+) signals during homeostatic plasticity |
title_short | Miro1‐dependent mitochondrial positioning drives the rescaling of presynaptic Ca(2+) signals during homeostatic plasticity |
title_sort | miro1‐dependent mitochondrial positioning drives the rescaling of presynaptic ca(2+) signals during homeostatic plasticity |
topic | Scientific Reports |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5286383/ https://www.ncbi.nlm.nih.gov/pubmed/28039205 http://dx.doi.org/10.15252/embr.201642710 |
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