Abstract
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.
Highlights
Newborns can interact with their environment soon after birth, without any previous experience of sensory input
We investigated the relationship between spontaneous activity and mitochondrial motility in vivo and in organotypic slice cultures of the developing mouse primary visual cortex during the second postnatal week before eye opening at postnatal day (P) 14 (Figure 1A)
Previous studies reported that neuronal activity and calcium signaling reduce mitochondrial motility in dendrites in vitro (Li et al, 2004; Chang et al, 2006), but this idea has not been tested in vivo
Summary
Newborns can interact with their environment soon after birth, without any previous experience of sensory input. Mitochondria are generated at the soma and transported to distal dendrites and axons via the microtubule network (Sheng and Cai, 2012). This motility allows for energy provision at high-e nergy-d emanding sites, in particular, synapses. A computational model of synaptic activity-m ediated control of mitochondrial motility suggests that the developmental increase in synapse number and transmission frequency contributes substantially to the age-dependent decrease of mitochondrial motility
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