Prolonged ethanol abuse has been associated with brain injury. In rodents, postnatal exposure to ethanol has been shown to be a major contributing factor to neurodegeneration in the hippocampus and cortex, leading to deficits in synaptic function and memory. Among the potential mechanisms involved in ethanol-induced brain damage, oxidative stress is considered a primary factor. However, the molecular mechanisms underlying ethanol-induced neurotoxicity remain incompletely understood. Evidence suggests that ethanol impairs the functions of both the cytoskeleton and cellular membranes, resulting in alterations to neuronal physiology. The plasma membrane of eukaryotic cells contains microdomains enriched in specific glycosphingolipids, gangliosides, and cholesterol, collectively forming membrane/lipid rafts (MLRs). As demonstrated in previous studies, MLRs function as scaffolds for a variety of molecular entities, including signaling receptors and ion channels. In addition, they mediate the organisation of the cytoskeleton. Indeed, numerous cytoskeletal components, their binding partners, and enzymes that regulate cytoskeletal dynamics localise to MLRs and contribute to the regulation of the lateral diffusion of membrane proteins and lipids in response to extracellular stimuli. The objective of the present research was to examine the effects of ethanol on the cytoskeleton, specifically actin and tubulin, in C6 glioma cells.