ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Metabolism regulates the spontaneous firing of substantia nigra pars reticulata neurons via KATP and nonselective cation channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Harnessing metabolic control for synaptic stability: REST/NRSF links glycolytic inhibition to excitatory neurotransmission.The Journal of physiology · 2025Article
- Low glycemic index diet restrains epileptogenesis in a gender-specific fashion.Cellular and molecular life sciences : CMLS · 2023Article
- Review
- Beta-Hydroxybutyrate: A Dual Function Molecular and Immunological Barrier Function Regulator.Frontiers in immunology · 2022Review
- Curbing action potential generation or ATP-synthase leads to a decrease in in-cell pyruvate dehydrogenase activity in rat cerebrum slices.Scientific reports · 2021Article
- Rheb mediates neuronal-activity-induced mitochondrial energetics through mTORC1-independent PDH activation.Developmental cell · 2021Article
- Neuromodulation or energy failure? Metabolic limitations silence network output in the hypoxic amphibian brainstem.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- GLP-1 Receptor Signaling in Astrocytes Regulates Fatty Acid Oxidation, Mitochondrial Integrity, and Function.Cell metabolism · 2020Article
- Nutritional ketosis as an intervention to relieve astrogliosis: Possible therapeutic applications in the treatment of neurodegenerative and neuroprogressive disorders.European psychiatry : the journal of the Association of European Psychiatrists · 2020Review
- Cellular and Synaptic Dysfunctions in Parkinson's Disease: Stepping out of the Striatum.Cells · 2019Review
- Quantitative in vivo imaging of neuronal glucose concentrations with a genetically encoded fluorescence lifetime sensor.Journal of neuroscience research · 2019Article
- Glycolytic inhibitor 2-deoxyglucose prevents cortical hyperexcitability after traumatic brain injury.JCI insight · 2019Article
- Ketogenic and anaplerotic dietary modifications ameliorate seizure activity in Drosophila models of mitochondrial encephalomyopathy and glycolytic enzymopathy.Molecular genetics and metabolism · 2019Article
- Lipid-independent control of endothelial and neuronal TRPC3 channels by light.Chemical science · 2019Article
- Population dynamics and entrainment of basal ganglia pacemakers are shaped by their dendritic arbors.PLoS computational biology · 2019Article
- Imaging pH Dynamics Simultaneously in Two Cellular Compartments Using a Ratiometric pH-Sensitive Mutant of mCherry.ACS omega · 2018Article
- Review
- The role of KActa pharmacologica Sinica · 2018Review
- BAD and KeLife · 2018Article
- Dysregulated Glucose Metabolism as a Therapeutic Target to Reduce Post-traumatic Epilepsy.Frontiers in cellular neuroscience · 2018Review
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Authors and funding
3 authors.
Funding
Abstract
Neurons use glucose to fuel glycolysis and provide substrates for mitochondrial respiration, but neurons can also use alternative fuels that bypass glycolysis and feed directly into mitochondria. To determine whether neuronal pacemaking depends on active glucose metabolism, we switched the metabolic fuel from glucose to alternative fuels, lactate or β-hydroxybutyrate, while monitoring the spontaneous firing of GABAergic neurons in mouse substantia nigra pars reticulata (SNr) brain slices. We found that alternative fuels, in the absence of glucose, sustained SNr spontaneous firing at basal rates, but glycolysis may still be supported by glycogen in the absence of glucose. To prevent any glycogen-fueled glycolysis, we directly inhibited glycolysis using either 2-deoxyglucose or iodoacetic acid. Inhibiting glycolysis in the presence of alternative fuels lowered SNr firing to a slower sustained firing rate. Surprisingly, we found that the decrease in SNr firing was not mediated by ATP-sensitive potassium (KATP) channel activity, but if we lowered the perfusion flow rate or omitted the alternative fuel, KATP channels were activated and could silence SNr firing. The KATP-independent slowing of SNr firing that occurred with glycolytic inhibition in the presence of alternative fuels was consistent with a decrease in a nonselective cationic conductance. Although mitochondrial metabolism alone can prevent severe energy deprivation and KATP channel activation in SNr neurons, active glucose metabolism appears important for keeping open a class of ion channels that is crucial for the high spontaneous firing rate of SNr neurons.
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