Acute ethanol exposure affects neuronal membrane receptors and intracellular kinases. At intoxicating concentrations (50–100 mM), acute ethanol activates type 1 dopamine receptor (DR1), adenylate cyclase and cAMP dependent protein kinase A (PKA) (Rabin et al., 1992; Lovinger, 2002; Ferrani-Kile et al., 2003; Moonat et al., 2010; Coller and Hutchinson, 2012), a signaling pathway closely related to synaptic plasticity (Eftekharzadeh et al., 2012; Nassireslami et al., 2013). Acute ethanol can also activate other intracellular kinases such as Akt/protein kinase B (PKB) signaling pathway (Carter et al., 2008; Neasta et al., 2011; Zeng et al., 2012) and glycogen synthase kinase 3 beta (GSK3β), both are multifunctional serine/threonine kinases (French and Heberlein, 2009; Luo, 2009; Zeng et al., 2012; Shah et al., 2015), required for synaptic plasticity (Horwood et al., 2006; Ochs et al., 2015). The involvement of these kinases in ethanol neurotoxicity provides a potential target for therapeutic efforts. Ethanol neurotoxicity can be reduced for example via inhibition of GSK3β activity (Shah et al., 2015).
