Direct effects of acute EtOH on the function of GPCRs and G proteins are generally weak. Furthermore, the physiologic impact of these actions is not always clear. However, there are mechanisms involving these molecules that are influenced by EtOH. Studies beginning in the 1980s showed that EtOH can stimulate cAMP formation (Luthin and Tabakoff 1984; Rabin and Molinoff 1981). This may be due to direct EtOH actions on AC, but other proteins that influence GPCRs and their signaling might play roles in the neural actions of EtOH (Bjork et al. 2008). The physiologic consequences of this AC activation have long been unclear. However, recent studies indicate that acute EtOH exposure can increase neurotransmitter release (described in greater detail later in this review, Fig. 1), and activation of AC is a strong candidate to mediate these effects (Kelm et al. 2008).
