addiction cycle. These stages have been linked to specific neural networks. For example, in regards to the Binge/Intoxication Stage, the acute reinforcing effects of alcohol are hypothesized to invoke the release of dopamine in the nucleus accumbens through its actions in the ventral tegmental area or nucleus accumbens). Candidate gene studies focused on neurotransmitters whose levels or end function are altered by the acute or chronic presence of alcohol have supported neuroimaging studies. As one example, dopamine (a key component of the brain’s reward circuitry) and serotonin (the primary contributor to motivation behaviors and mood) are considered to be among alcohol’s major liability factors. Alcohol’s ability to modulate dopamine levels results in neuronal adaptation that perpetuates further alcohol/other drug use. Although the different mechanisms by which alcohol evokes its acute reinforcing effects on the brain remain poorly understood, its effects appear to be mediated by the actions of the dopamine, serotonin, opioid, and GABA systems in the basal forebrain. For instance, alcohol use leads to the release of endogenous opioids, which activate mu-opioid receptors on GABAergic interneurons in the ventral tegmental area, resulting in attenuation of inhibitory tone from these onto mesolimbic dopamine-neurons, and ultimately increased dopamine release in the
