Addictive behaviour associated with alcoholism is a brain disease characterized by craving for alcohol, loss of control over consumption, development of tolerance and dependence, while simultaneously the repertoire of social functioning not related to intake behaviour declines dramatically. To understand the factors that compel some individuals to drink excessively and to identify targets for pharmacological intervention, addiction research has focused on the identification of brain mechanisms that support reinforcing actions of alcohol and the progression of changes in neural function induced by chronic drug or ethanol intake. Cellular and molecular mechanisms of tolerance, sensitization, and dependence have been investigated intensively. The ability of most drugs to enhance dopamine neurotransmission particularly within the mesocorticolimbic dopamine (“reward”) system was demonstrated repeatedly. However, the past decade has placed the dopamine system within a broader context of neuronal circuitry involved in drug seeking, drug taking, and recovery. Specific effects on other receptors symptoms provide particular challenges given the almost ubiquitous expression of these receptors throughout the CNS. Additionally, new emphasis on various neuropeptide systems has reemerged, including opioid peptides and the stress-related peptides of the hypothalamus-pituitary-adrenal axis. Continued research is warranted on the various neurobiological based components that underlie the transition from drug intake to addiction to define drug targets for innovative pharmacological treatment options.