ArticleThe Journal of cell biology2024
Sirtuin3 ensures the metabolic plasticity of neurotransmission during glucose deprivation.
Article in The Journal of cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- 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
- Mitochondrial CaNature metabolism · 2026Article
- Advances in the Development of Mitochondrial Pyruvate Carrier Inhibitors for Therapeutic Applications.Biomolecules · 2025Review
- Mitochondrial pyruvate transport regulates presynaptic metabolism and neurotransmission.Science advances · 2024Article
- Neuronal activity-driven O-GlcNAcylation promotes mitochondrial plasticity.Developmental cell · 2024Article
- Review
- Mitochondrial pyruvate transport regulates presynaptic metabolism and neurotransmission.bioRxiv : the preprint server for biology · 2024Article
- Sirtuin3 ensures the metabolic plasticity of neurotransmission during glucose deprivation.The Journal of cell biology · 2024Article
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10 authors at 1 institution in 1 country.
Funding
Abstract
Neurotransmission is an energetically expensive process that underlies cognition. During intense electrical activity or dietary restrictions, the glucose level in the brain plummets, forcing neurons to utilize alternative fuels. However, the molecular mechanisms of neuronal metabolic plasticity remain poorly understood. Here, we demonstrate that glucose-deprived neurons activate the CREB and PGC1α transcriptional program, which induces expression of the mitochondrial deacetylase Sirtuin 3 (Sirt3) both in vitro and in vivo. We show that Sirt3 localizes to axonal mitochondria and stimulates mitochondrial oxidative capacity in hippocampal nerve terminals. Sirt3 plays an essential role in sustaining synaptic transmission in the absence of glucose by providing metabolic support for the retrieval of synaptic vesicles after release. These results demonstrate that the transcriptional induction of Sirt3 facilitates the metabolic plasticity of synaptic transmission.
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Registered trials
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