Ingested alcohol, primarily in the form of ethanol, likely affects excitability of neurons, potentially through indirect effects on metabolism (Volkow et al., 2015, Volkow et al., 2017) (Fig. 1G). Slice recordings of mouse brain have revealed that acute application of ethanol enhances firing of dopamine neurons of the ventral tegmental area (VTA) (Brodie et al., 1999), lateral habenula neurons and cerebellar Golgi neurons, while decreasing the firing of VTA GABA-releasing (GABAergic) neurons (Gallegos et al., 1999), pyramidal neurons in the lateral orbitofrontal cortex (Nimitvilai-Roberts et al., 2021), and serotonergic neurons of the dorsal raphe (Maguire et al., 2014). Several studies have also reported changes in excitability following chronic exposure to ethanol. Firing was increased in mouse nucleus accumbens (NAc) medium spiny neurons recorded after long-term ethanol self-administration (Hopf et al., 2010). Similarly, repeated systemic ethanol treatment increased spontaneous action potential firing in mouse lateral habenula (LHb) neurons (Agrawal et al., 2012). Due to its amphipathic nature, ethanol can easily cross the blood brain barrier (BBB) and any cell membrane lipid bilayer (Kumari et al., 2018) directly affecting multiple molecular targets
