observed in sphingomyelin–DOPE bilayers [47]. One suggestion to explain this effect is that acute molecular tolerance to ethanol involves interaction with multiple sites perhaps with opposing (i.e. potentiating versus inhibiting) effects within the BK channel, and changes in lipid environment selectively alter ethanol access to these sites [47]. The activity of BK channels is influenced by the cholesterol/phospholipid ratio and the composition in the surrounding lipid bilayer [48]. Ethanol activation of BK channels is modulated by the cholesterol content in lipid bilayers [49] and certain structural features of phospholipids (such as molecular shape) influence the ethanol response [11].
