ArticleThe Journal of biological chemistry2015
The role of mitochondrially derived ATP in synaptic vesicle recycling.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 2 of them syntheses that pooled it.
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Who cites it
181 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Bioenergetic impairment in schizophrenia: role of mitochondrial signaling in synaptic dysfunction - a systematic review.Frontiers in cell and developmental biology · 2026Pooled it
- Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria.Ageing research reviews · 2022Pooled it
- Mitochondrial molecular diversity in the brain.Current opinion in neurobiology · 2026Review
- Mitochondrial calcium influx-driven bioenergetics selectively enable drug addiction.Nature neuroscience · 2026Article
- Reduced expression of Brain Expressed X-linked genes in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Article
- Brain mitochondria as key drivers of cognition and behaviour.Nature reviews. Neuroscience · 2026Review
- The therapeutic effect of nicotinamide riboside chloride on ameliorating alcohol-induced neuronal damage with a focus on mitochondrial unfolded protein response and mitophagy.Genes & diseases · 2026Article
- Article
- CTRP10 is required for optimal motor function.The Journal of biological chemistry · 2026Article
- A fistful of iron: ferritin as a vulnerability point of the brain cancers.Cell death & disease · 2026Review
- Early Reduction in Mitochondrial Membrane Potential in Synaptic Mitochondria Contribute to Synaptic Pathology in the EAE Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2026Article
- Optimal neuromuscular performance requires motor neuron phosphagen kinases.The Journal of physiology · 2026Article
- From oversight to insight: the curious case of the endothelial insulin receptor.Blood vessels, thrombosis & hemostasis · 2026Review
- Mitochondrial CaNature metabolism · 2026Article
- Mitochondrial CaBiomolecules · 2026Review
- A central role for PINK1 in governing local mitochondrial biogenesis and degradation in neurons.Cellular and molecular life sciences : CMLS · 2026Review
- Direct energy consumption by inhibitory GABAFrontiers in neuroscience · 2026Article
- Synaptic mitochondrial dysfunction and Alzheimer's disease: from molecular mechanisms to therapeutic strategies.Frontiers in pharmacology · 2026Review
- Beyond lifespan and healthspan: a biological framework for experienced longevity.Frontiers in aging neuroscience · 2026Article
- Controlling interfacial protein adsorption, desorption and aggregation in biomolecular condensates.Nature communications · 2025Article
121 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors.
Funding
Abstract
Synaptic mitochondria are thought to be critical in supporting neuronal energy requirements at the synapse, and bioenergetic failure at the synapse may impair neural transmission and contribute to neurodegeneration. However, little is known about the energy requirements of synaptic vesicle release or whether these energy requirements go unmet in disease, primarily due to a lack of appropriate tools and sensitive assays. To determine the dependence of synaptic vesicle cycling on mitochondrially derived ATP levels, we developed two complementary assays sensitive to mitochondrially derived ATP in individual, living hippocampal boutons. The first is a functional assay for mitochondrially derived ATP that uses the extent of synaptic vesicle cycling as a surrogate for ATP level. The second uses ATP FRET sensors to directly measure ATP at the synapse. Using these assays, we show that endocytosis has high ATP requirements and that vesicle reacidification and exocytosis require comparatively little energy. We then show that to meet these energy needs, mitochondrially derived ATP is rapidly dispersed in axons, thereby maintaining near normal levels of ATP even in boutons lacking mitochondria. As a result, the capacity for synaptic vesicle cycling is similar in boutons without mitochondria as in those with mitochondria. Finally, we show that loss of a key respiratory subunit implicated in Leigh disease markedly decreases mitochondrially derived ATP levels in axons, thus inhibiting synaptic vesicle cycling. This proves that mitochondria-based energy failure can occur and be detected in individual neurons that have a genetic mitochondrial defect.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.