Binding of endogenous acetylcholine (ACh) or nicotine induces a conformational change of the receptor allowing for an influx of cations (Ca2+, Na+, or K+ depending on nAChR subtype) through the central channel for a few milliseconds, followed by a non-conducting closed receptor state (Giniatullin et al., 2005). In contrast, ethanol is not a direct agonist at nAChRs but can potentiate the response of these receptors to Ach (Aistrup et al., 1999; Cardoso et al., 1999; Zuo et al., 2002). The pharmacological properties of the nAChRs to agonists such as ACh, nicotine or ethanol is highly dependent on its subunit composition and location of the receptor (Yu et al., 1996; Pidoplichko et al., 1997; Cardoso et al., 1999; Wooltorton et al., 2003).
