The metabolism of ethanol within neurons has been an area of relative understudy, notwithstanding the recognized influence of alterations in neuronal metabolism on their functional activity. Recent investigations indicate a preferential utilization of ethanol over glucose as a carbon and energy source by neurons, inducing a reprogramming effect that leads to a diminished energy potential and reduced capacity to utilize glucose once ethanol reserves are depleted. Notably, ethanol intake is associated with discernible alterations in neuronal firing, and specific electroencephalogram (EEG) patterns have been identified as indicators of susceptibility to alcohol use disorder (AUD). Furthermore, a specific haplotype of the inwardly rectifying potassium channel subunit, GIRK2, pivotal in regulating neuronal excitability, has been implicated in AUD and demonstrated to be directly modulated by ethanol. Conversely, the overexpression of GIRK2 has been found to mitigate ethanol-induced metabolic changes. In light of the available evidence, it is discerned that the elucidation of mechanisms governing ethanol’s impact on neuronal metabolism represents a promising novel target for the development of therapeutic interventions for AUD.
Popova, D., Sun, J., Chow, H. M., & Hart, R. P. (2024). A critical review of ethanol effects on neuronal firing: A metabolic perspective. Alcohol, clinical & experimental research, 10.1111/acer.15266. Advance online publication. https://doi.org/10.1111/acer.15266