Pharmacology of Alcohol and Alcohol Use Disorder

Alcohol (ethanol) is a central nervous system (CNS) depressant drug that, depending on its blood concentration, can induce various manifestations such as relief from anxiety, disinhibition, ataxia, and general anesthesia. Chronic exposure to alcohol can cause persistent structural and functional changes in the brain. Since alcohol is widely abused and alcohol dependence often leads to serious medical and social problems, medication is very important. It is crucial that we understand the complex mechanism of action of alcohol to find better therapeutic alternatives. Alcohol acts on various neurotransmitters such as gamma-aminobutyric acid (GABA), glutamate, dopamine, serotonin, and endogenous opioids. Alcohol is both a GABA agonist and a glutamate N-methyl-Daspartate (NMDA) receptor antagonist. It also facilitates dopamine release from the nucleus accumbens, although the effect is not potent. Its actions on dopaminergic and opioid peptidergic systems are implicated in the reinforcing effect of alcohol. After chronic exposure, downregulation of GABAergic and upregulation of NMDA glutamatergic systems typically occur. Normalizing this imbalance might be effective in the treatment of alcohol dependence. Antagonism of the µ-opioid system also reduces the motivation to consume alcohol. New animal models of binge alcohol intake, such as the alcohol deprivation effect (ADE) and the “Drinking-in-the-Dark” technique, would help us to develop new treatment methods against alcohol dependence. In this chapter, neurobehavioral effects of both acute and chronic alcohol exposure are described. In addition, some recent advancements in biomedical research are introduced with reference to hepatic and cardiovascular influences of alcohol, factors relevant to the development of alcohol dependence, and biological targets for the treatment of alcohol dependence. © Springer Nature Switzerland AG 2022.