ArticleCell2014
Activity-driven local ATP synthesis is required for synaptic function.
Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 494 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
494 citing papers in PubMed, 1 synthesis or guideline pooled it, 821 citations in OpenAlex.
- Bioenergetic impairment in schizophrenia: role of mitochondrial signaling in synaptic dysfunction - a systematic review.Frontiers in cell and developmental biology · 2026Pooled it
- The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Vagal nerve stimulation induces vascular oscillations and enhances long-term learning.iScience · 2026Article
- Disrupted TFEB/GDNF-cAMP/ATP Coupling Underlies Astrocytic Dysfunction and Depression in LRRK2 G2019S Parkinson's Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondrial calcium influx-driven bioenergetics selectively enable drug addiction.Nature neuroscience · 2026Article
- 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
- Aberrant protein S-nitrosylation disrupts axonal development and metabolic homeostasis in a Cntnap2 mouse model of autism.Redox biology · 2026Article
- Brain mitochondria as key drivers of cognition and behaviour.Nature reviews. Neuroscience · 2026Review
- Reduced expression of Brain Expressed X-linked genes in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Article
- Kinetic Control of Nuclear-encoded Mitochondrial mRNA Localization and Local Translation.bioRxiv : the preprint server for biology · 2026Article
- Enhanced axonal mitochondrial motility and neural activity-induced energy deficits destabilize synaptic transmission in models of bipolar disorder.Nature communications · 2026Article
- A Caudate Pathway-level Transcriptomic Signature of Translational, Bioenergetic, and Proteostatic Programs in Obsessive-compulsive Disorder.Journal of molecular neuroscience : MN · 2026Article
- Activity-dependent protein synthesis in neurons requires microglial-metabolic coupling.Cell metabolism · 2026Article
- Asymmetric distribution of mitochondrial CaExperimental & molecular medicine · 2026Article
- Quantitative In Vivo Imaging of ATP Dynamics in Drosophila Using the Ratiometric Biosensor QUEEN.Development, growth & differentiation · 2026Article
- Cholesterol at the Center of Alzheimer's Disease: A Unifying Hypothesis on the Pathogenic Mechanism.Molecules (Basel, Switzerland) · 2026Review
- Altered hypothalamic metabolism in chronic cluster headache patients measured withThe journal of headache and pain · 2026Article
- Mitochondrial calcium modulates odor-mediated behavioral plasticity in Caenorhabditis elegans.Molecules and cells · 2026Article
- Polarized mitochondrial respiratory chain complexes in synaptic mitochondria induced by plasticity signals.Molecular and cellular biochemistry · 2026Article
- Focused Ultrasound Modulation of PGC-1α Pathways in Neurological Disease: Mechanistic Rationale and Translational Opportunities.Molecular neurobiology · 2026Review
434 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cognitive function is tightly related to metabolic state, but the locus of this control is not well understood. Synapses are thought to present large ATP demands; however, it is unclear how fuel availability and electrical activity impact synaptic ATP levels and how ATP availability controls synaptic function. We developed a quantitative genetically encoded optical reporter of presynaptic ATP, Syn-ATP, and find that electrical activity imposes large metabolic demands that are met via activity-driven control of both glycolysis and mitochondrial function. We discovered that the primary source of activity-driven metabolic demand is the synaptic vesicle cycle. In metabolically intact synapses, activity-driven ATP synthesis is well matched to the energetic needs of synaptic function, which, at steady state, results in ∼10(6) free ATPs per nerve terminal. Despite this large reservoir of ATP, we find that several key aspects of presynaptic function are severely impaired following even brief interruptions in activity-stimulated ATP synthesis.
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What OpenQuestion holds
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.