A critical review of ethanol effects on neuronal firing: A metabolic perspective.
paper
Primary
Public
- Authors
- Popova, Dina; Sun, Jacquelyne; Chow, Hei-Man; Hart, Ronald P
- Year
- 2024
- Journal
- Alcohol, clinical & experimental research
- PMID
- 38217065
- DOI
- 10.1111/acer.15266
- PMCID
- PMC10966925
Ethanol metabolism is relatively understudied in neurons, even though changes in neuronal metabolism are known to affect their activity. Recent work demonstrates that ethanol is preferentially metabolized over glucose as a source of carbon and energy, and it reprograms neurons to a state of reduced energy potential and diminished capacity to utilize glucose once ethanol is exhausted. Ethanol intake has been associated with changes in neuronal firing and specific brain activity (EEG) patterns have been linked with risk for alcohol use disorder (AUD). Furthermore, a haplotype of the inwardly rectifying potassium channel subunit, GIRK2, which plays a critical role in regulating excitability of neurons, has been linked with AUD and shown to be directly regulated by ethanol. At the same time, overexpression of GIRK2 prevents ethanol-induced metabolic changes. Based on the available evidence, we conclude thatΒ the mechanisms underlying the effects of ethanol on neuronal metabolism are a novel target for developing therapies for AUD.
Metabolism of ethanol in neurons.Summary of metabolic pathways affected by ethanol utilization in neurons. See text for detailed description. A. Ethanol conversion to acetate, via CAT and CYP2E1 but reduced activity of ADH (indicated by grey text). B. Acetyl-CoA serves as input for the tricarboxylic acid (TCA) cycle. C. Reduced glucose utilization due to down-regulation of PFK1 (indicated by grey text and arrows). D. Reduced glucose uptake due to inhibition of AMPK regulation of glucose transporter expression (GLUT1,3,4). E. Pyruvate, potentially derived from astrocytic lactate, as source for multiple TCA intermediates. F. Production of glutamate (Glu) and gamma acetyl butyric acid (GABA) draws carbons from the TCA cycle, reducing NADH and, ultimately, ATP production. G. Neuronal depolarization exports potassium ions and imports sodium ions, which required energy to restore normal gradients. H. G-protein linked, inwardly rectifying potassium channel (GIRK) is a target of ethanol, affecting neuronal activity.
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