TY - JOUR
T1 - Activity-dependent regulation of mitochondrial motility in developing cortical dendrites
AU - Silva, Catia Ap
AU - Yalnizyan-Carson, Annik
AU - Fernández Busch, M. Victoria
AU - van Zwieten, Mike
AU - Verhage, Matthijs
AU - Lohmann, Christian
N1 - Publisher Copyright: © 2021, Silva et al. Copyright: This record is sourced from MEDLINE/PubMed, a database of the U.S. National Library of Medicine
PY - 2021/9/7
Y1 - 2021/9/7
N2 - 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.
AB - 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.
KW - calcium signaling
KW - in vivo imaging
KW - intracellular transport
KW - mouse
KW - neuroscience
KW - synaptic transmission
UR - http://www.scopus.com/inward/record.url?scp=85115917157&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85115917157&partnerID=8YFLogxK
U2 - https://doi.org/10.7554/eLife.62091
DO - https://doi.org/10.7554/eLife.62091
M3 - Article
C2 - 34491202
SN - 2050-084X
VL - 10
JO - eLife
JF - eLife
M1 - e62091
ER -