Activity-dependent regulation of mitochondrial motility in developing cortical dendrites

Developing neurons form synapses at a high rate. Synaptic transmission is very energy-demanding and likely requires ATP production by mitochondria nearby. Mitochondria might be targeted to active synapses in young dendrites, but whether such motility regulation mechanisms exist is unclear. We invest...

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Autores principales:	Catia AP Silva, Annik Yalnizyan-Carson, M Victoria Fernández Busch, Mike van Zwieten, Matthijs Verhage, Christian Lohmann
Formato:	article
Lenguaje:	EN
Publicado:	eLife Sciences Publications Ltd 2021
Materias:	in vivo imaging synaptic transmission intracellular transport calcium signaling Medicine R Science Q Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/8e00e2bafc1f46d9be301460c1555bff
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id	oai:doaj.org-article:8e00e2bafc1f46d9be301460c1555bff
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spelling	oai:doaj.org-article:8e00e2bafc1f46d9be301460c1555bff2021-11-24T12:24:59ZActivity-dependent regulation of mitochondrial motility in developing cortical dendrites10.7554/eLife.620912050-084Xe62091https://doaj.org/article/8e00e2bafc1f46d9be301460c1555bff2021-09-01T00:00:00Zhttps://elifesciences.org/articles/62091https://doaj.org/toc/2050-084XDeveloping neurons form synapses at a high rate. Synaptic transmission is very energy-demanding and likely requires ATP production by mitochondria nearby. Mitochondria might be targeted to active synapses in young dendrites, but whether such motility regulation mechanisms exist is unclear. We investigated the relationship between mitochondrial motility and neuronal activity in the primary visual cortex of young mice in vivo and in slice cultures. During the first 2 postnatal weeks, mitochondrial motility decreases while the frequency of neuronal activity increases. Global calcium transients do not affect mitochondrial motility. However, individual synaptic transmission events precede local mitochondrial arrest. Pharmacological stimulation of synaptic vesicle release, but not focal glutamate application alone, stops mitochondria, suggesting that an unidentified factor co-released with glutamate is required for mitochondrial arrest. A computational model of synaptic transmission-mediated mitochondrial arrest shows that the developmental increase in synapse number and transmission frequency can contribute substantially to the age-dependent decrease of mitochondrial motility.Catia AP SilvaAnnik Yalnizyan-CarsonM Victoria Fernández BuschMike van ZwietenMatthijs VerhageChristian LohmanneLife Sciences Publications Ltdarticlein vivo imagingsynaptic transmissionintracellular transportcalcium signalingMedicineRScienceQBiology (General)QH301-705.5ENeLife, Vol 10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	in vivo imaging synaptic transmission intracellular transport calcium signaling Medicine R Science Q Biology (General) QH301-705.5
spellingShingle	in vivo imaging synaptic transmission intracellular transport calcium signaling Medicine R Science Q Biology (General) QH301-705.5 Catia AP Silva Annik Yalnizyan-Carson M Victoria Fernández Busch Mike van Zwieten Matthijs Verhage Christian Lohmann Activity-dependent regulation of mitochondrial motility in developing cortical dendrites
description	Developing neurons form synapses at a high rate. Synaptic transmission is very energy-demanding and likely requires ATP production by mitochondria nearby. Mitochondria might be targeted to active synapses in young dendrites, but whether such motility regulation mechanisms exist is unclear. We investigated the relationship between mitochondrial motility and neuronal activity in the primary visual cortex of young mice in vivo and in slice cultures. During the first 2 postnatal weeks, mitochondrial motility decreases while the frequency of neuronal activity increases. Global calcium transients do not affect mitochondrial motility. However, individual synaptic transmission events precede local mitochondrial arrest. Pharmacological stimulation of synaptic vesicle release, but not focal glutamate application alone, stops mitochondria, suggesting that an unidentified factor co-released with glutamate is required for mitochondrial arrest. A computational model of synaptic transmission-mediated mitochondrial arrest shows that the developmental increase in synapse number and transmission frequency can contribute substantially to the age-dependent decrease of mitochondrial motility.
format	article
author	Catia AP Silva Annik Yalnizyan-Carson M Victoria Fernández Busch Mike van Zwieten Matthijs Verhage Christian Lohmann
author_facet	Catia AP Silva Annik Yalnizyan-Carson M Victoria Fernández Busch Mike van Zwieten Matthijs Verhage Christian Lohmann
author_sort	Catia AP Silva
title	Activity-dependent regulation of mitochondrial motility in developing cortical dendrites
title_short	Activity-dependent regulation of mitochondrial motility in developing cortical dendrites
title_full	Activity-dependent regulation of mitochondrial motility in developing cortical dendrites
title_fullStr	Activity-dependent regulation of mitochondrial motility in developing cortical dendrites
title_full_unstemmed	Activity-dependent regulation of mitochondrial motility in developing cortical dendrites
title_sort	activity-dependent regulation of mitochondrial motility in developing cortical dendrites
publisher	eLife Sciences Publications Ltd
publishDate	2021
url	https://doaj.org/article/8e00e2bafc1f46d9be301460c1555bff
work_keys_str_mv	AT catiaapsilva activitydependentregulationofmitochondrialmotilityindevelopingcorticaldendrites AT annikyalnizyancarson activitydependentregulationofmitochondrialmotilityindevelopingcorticaldendrites AT mvictoriafernandezbusch activitydependentregulationofmitochondrialmotilityindevelopingcorticaldendrites AT mikevanzwieten activitydependentregulationofmitochondrialmotilityindevelopingcorticaldendrites AT matthijsverhage activitydependentregulationofmitochondrialmotilityindevelopingcorticaldendrites AT christianlohmann activitydependentregulationofmitochondrialmotilityindevelopingcorticaldendrites
_version_	1718415059109019648

Activity-dependent regulation of mitochondrial motility in developing cortical dendrites

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