The pharmacodynamics of alcohol and marijuana are the subject of study in several empirical works examining their physiological and behavioral effects. Chronic alcohol exposure is associated with cortical and white matter volume loss secondary to decreases in choline and N-acetyl aspartate, reduced GABAa receptor efficacy, and impaired neurogenesis (Crews et al. 2005; Meyerhoff et al. 2004). Similarly, the principal active component of marijuana, delta9-tetrahydrocannabinol (delta9-THC), produces complex alterations in cognition and behavior that involve several neuronal substrates (Fant et al. 1998; Johns 2001; Solowij et al. 2002). Brain regions with high densities of CB-1 receptors, and thus susceptible to the effects of THC, include the frontal regions, hippocampus, basal ganglia, cerebellum, amygdala, and striatum (Freedland et al. 2002; Iversen 2003; Pontieri et al. 1999; Quickfall and Crockford 2006). Human studies examining CNS sequelae of chronic marijuana use provide evidence for increased metabolism (Block et al. 2000; Mathew et al. 2002) and activation of alternate neural pathways within these regions (Eldreth et al. 2004; Kanayama et al. 2004). Further adverse effects may result from the pharmacological interaction of alcohol and marijuana,
