of the dorsal striatum during alcohol addiction is thought to help to solidify habitual behaviors associated with drug seeking and taking. Namely, neuroadaptations in the dorsal striatum involve changes in glutamate, GABA and the endocannabinoid system (Koob and Volkow, 2010). After a period of repeated binge/intoxication neuroadaptations occur leading to a negative emotional state (e.g., anxiety, depression, anhedonia) induced by alcohol withdrawal. Negative reinforcement mechanisms predominately drive behavior where motivation to continue excessive consumption is strengthened by the alleviation of negative affect by resumed alcohol drinking. Neuroadaptations in the brain reward and stress systems (e.g., extended amygdala) drive dependent (compulsive) drinking. Neuroadaptations occurring in the circuitry of the mesolimbic dopamine system, particularly the ventral tegmental area (VTA), the nucleus accumbens (NAc), and amygdala, cause enhanced saliency value of the drug and drug stimuli, and the decreased sensitivity to natural reinforcers. For example, decreases in dopamine and GABA system function, and increases in dynorphin-κ opioid activity in the ventral striatum, representing a general decrease in reward system function (within-system opponent processes), are coupled with enhancement of cortioctropin-releasing factor (CRF) in the extended amygdala as well as blunting of the hypothalamic–pituitary–adrenal (HPA) axis (between-system opponent processes). Finally, compulsive dependent consumption involves poor
