Ethanol Effects on the Cytoskeleton of Nerve Tissue Cells

Ethanol (EtOH) is the most ancient drug and one of those most used and abused by human beings. Although its effects are better known and are best studied on the cytoskeleton of hepatocytes (due to the EtOH role in the etiology of liver cirrhosis), its effects on nerve tissue cells' cytoskeleton are beginning to be elucidated. We review in this chapter the known mechanisms by which EtOH affects microtubules, intermediate filaments, and microfilaments. EtOH disrupts the cytoskeleton in many different and still incompletely known ways (spontaneous chemical reactions with derivatives of EtOH metabolism, changes in the expression level of cytoskeletal proteins, functional modification of proteins with regulatory actions on cytoskeleton assembly or disassembly, etc.). EtOH's deleterious effects, by acting on neuronal and glial cytoskeleton during embryonic and/or fetal development, are a critical factor in the induction of alcohol-related neurodevelopmental disorders (ARND) and fetal alcohol syndrome (FAS). Its cytoskeletal actions during adulthood are also critical in the induction of different neuropsychiatric disorders (such as alcoholic dementia). However, existing evidence points to the fact that EtOH disruption of cytoskeleton in neurons is shared with the effects of other noxious stimuli (hypoxia-asphyxia, traumatic brain injuries, electrical discharges, neurotoxicants, other drugs of abuse, neurodegenerative disorders, etc.). We propose here that a presently forgotten and disregarded (but classically described) form of chronic neuronal disease (Zellschrumpfung) is an ancient morphological evidence of neuronal cytoskeletal involvement in the action of those many noxious stimuli. Taking into account all the existing present and historical evidence, we may conclude that the damage to the cytoskeleton is a common final pathway for neuronal damage.