Social Science

A Single Alcoholic Beverage May Alter Brain Cells’ Mitochondrial Function Permanently

A Single Alcoholic Beverage May Alter Brain Cells’ Mitochondrial Function Permanently

According to new research, a single exposure to ethanol causes permanent changes to the neurons in both fruit flies and mice, leading to synaptic remodeling in the brain’s reward circuit. One alcoholic drink may set the brain up to develop a later alcohol addiction, according to a study published in the journal PNAS.

The neural mechanisms that mediate the change from occasional drinking to full-blown alcoholism are poorly understood. The authors of the study set out to investigate the molecular, cellular, and behavioral impacts of a single dose of alcohol in two species that are frequently used as models for studying the human brain in order to learn more about this precarious slope.

The scientists examined more than 2,000 hippocampus proteins in the brains of mice after ethanol exposure using quantitative mass spectrometry. They discovered 72 proteins in all that drinking alcohol significantly changed.

For instance, modifications to the proteins MAP6 and ankyrin-G led to a reduction in the length of the crucial axon beginning segment of neuronal connecting arms for at least 24 hours after exposure. The researchers also noticed a considerable increase in the migration of mitochondria into ethanol-treated mouse neurons.

This increase in migration is expected to have a significant effect on the way that these neurons function because mitochondria supply energy to nerve cells. This shows that a single alcohol injection may result in substantial changes within the brain that could pave the way for alcoholism, along with the morphological changes seen in nerve cells exposed to ethanol.

The authors of the study state that some of the morphological alterations caused by ethanol “may potentially impair ethanol-related memory formation by disrupting the synaptic connection balance.”

They attempted to undo these cellular effects on fruit flies that had become tolerant to ethanol in order to test this theory. The scientists stopped the animals’ reliance on alcohol by blocking the proteins that regulate the migration of mitochondria into dopamine neurons.

Such a discovery would seem to support the idea that the neurology of addiction is truly driven by the cellular alterations seen after a single ethanol dose. It is remarkable that the development of ethanol addiction in both fruit flies and humans depends on dopamine neurons, though additional research is required to discover whether this holds true for humans.

According to research author Henrike Scholz, “it is interesting that the biological processes contributing to such intricate reward behavior are maintained across species, suggesting a similar role in humans.” These mechanisms may even be pertinent to the discovery that early alcohol consumption in humans is a significant risk factor for later alcohol consumption and the emergence of alcohol addiction.

This means that the first step in understanding how acute drinking can develop into chronic alcohol consumption is to detect long-lasting ethanol-dependent alterations.