In 2014, it was estimated that brain diseases were responsible for 35% of Europe’s disease burden, with addictions having the 4th most cases after anxiety disorders, migraine and mood disorders (DiLuca & Olesen, 2014). Therefore, it is important to find out addiction mechanisms, which in many countries such as in Finland are mainly due to alcohol use disorders (AUDs). The significance of alcohol diseases to individuals and the society is vast. Alcohol use on the 21st century has been estimated to cost about 2.6% of the gross domestic product (Manthey et al., 2021), with about one third being direct costs and the rest due to loss of productivity.

Fifty years ago, alcohol was shown to affect cell membranes (Curran & Seeman, 1977), a theory that was replaced by the receptor protein theory by Franks and Lieb (Franks & Lieb, 1982). Ethanol (ethyl alcohol, here often “alcohol”) does not have a single receptor target like some sedative drugs such as barbiturates and benzodiazepines (BZs) have, and still these drugs often have similar behavioral and emotional effects as alcohol in man and rodents. Barbiturates and BZs have their main targets on γ-aminobutyric acid type A receptors (GABAAR) (Korpi, Grunder, & Luddens, 2002), the main fast-acting inhibitory neurotransmitter receptor system in mammalian brains (Seeburg, Wisden, Verdoorn, Pritchett, Werner, Herb et al., 1990). The GABA system is among the targets through which ethanol actions are mediated, which will be reviewed here with the ultimate idea of understanding its possible role in the treatment of AUDs.