go task. Thus, although the study found no differences in delay discounting, the mice bred for higher alcohol consumption had impaired response inhibition on at least one measure. Such response inhibition data are consistent with Logue, Swartz, & Wehner (1998), who assessed the genetic relationship between nose poking efficiency and subsequent consumption of a 10% ethanol solution vs. water in a 2-bottle choice procedure, using 13 inbred strains of mice. Strains that confined their nose poking to periods when it yielded rewards (more efficient behavior) also consumed less ethanol. Logue and colleagues interpreted this as indicating a genetic relationship between impulsivity and ethanol consumption. Using the same procedure, Bowers & Wehner (2001) found that mice evidencing the gene encoding the neuronal-specific γ subtype of protein kinase C (PKCγ) consumed more alcohol and also demonstrated increased impulsivity in an appetitive-signaled nose poke task when compared with control mice. PKCγ may be an important mechanism within the cell that mediates one or more neurochemical pathways relevant to an increased predisposition to alcoholism and behavioral impulsivity (Bowers & Wehner, 2001). Studies delineating additional mechanisms underlying these genetically-based relationships between impulsivity and propensity to develop AUDs will be an important future research direction.
