influence of alcohol. A testable assumption is that different drinking patterns will elicit different varieties of tolerance. For example, characteristics of tolerance produced by drinking that is ‘massed’ (i.e. long drinking bouts) versus ‘spaced’ (i.e. shorter, intermittent bouts of drinking) might produce different types of tolerance, analogous to memories with different characteristics produced by spaced versus massed learning sessions [80]. Ethanol, via both direct and indirect activation of dopaminergic neurons in the ventral tegmental area [7,81], increases dopamine release in the striatum, which has been linked to both motivational and locomotor properties of most abused drugs. Although ion channels are the essential building blocks underlying neuronal activity and behaviors, it will be difficult to understand a complex behavioral trait such as alcohol addiction by simply focusing on the level of individual molecules. Clearly, ignoring the importance of brain circuitry in determining the behavioral inclination towards destructive drinking would be unwise. Depression, similar to alcohol addiction, represents a complex behavioral state, yet an understanding of the role of serotonin reuptake in this disorder has been helpful in the development of the selective serotonin reuptake inhibitors (SSRIs) effective in treatment. Understanding the actions of alcohol at the level of an individual BK
