DA release stimulated by systemic administration of ethanol. It has been postulated that ethanol's actions in the NAc may facilitate the release of endogenous ACh in the VTA, leading to activation of nAChRs and consequently elevating accumbal DA release (Larsson et al., 2005). In support, voluntary ethanol intake in rats has been shown to cause a significant increase in ACh levels in the VTA which is time-locked with the DA increase in the NAc (Larsson et al., 2005). It should be mentioned here that in addition to nAChRs, ethanol is known to modulate DA neurotransmission through actions at other molecular targets [for review (Vengeliene et al., 2008)]. For example, ethanol (10–80 mM) acting on pre-synaptic D1 receptors can increase excitatory glutamate transmission in the VTA and enhance DA release (Xiao et al., 2009).
