As described in the Koob and Volkow model (
2016), most drugs of abuse result in the hyperactivation of the mesocorticolimbic dopaminergic reward pathway in the binge-intoxication stage of addiction. This hyperactivation seems to be present in cannabis addiction but to a lower extent. Acute THC administration elicits striatal DA release in animals (Bloomfield et al.
2016) and THC challenges were shown to increase striatal DA transmission in humans (Stokes et al.
2010; Bossong et al.
2015); although other studies have found no THC-induced increases in striatal DA (Barkus et al.
2011; Urban et al.
2012). Additionally, there are no baseline differences in dopamine D2/D3 receptor availability between cannabis users and healthy controls (Volkow et al.
2014c; van de Giessen et al.
2017), a finding that does not parallel addiction to other drugs of abuse (including cocaine, alcohol, methamphetamine, nicotine, or heroin) which is associated with substantial reductions in D2R availability in the ventral striatum (Wang et al.
1997; Volkow et al.
2001,
2014c,
2017c; Martinez et al.
2012; Albrecht et al.
2013; Tomasi et al.
2015a; Wiers et al.
2016a; Ashok et al.
2017). Nonetheless, as with other drugs of abuse, chronic cannabis use still results in blunted dopamine reactivity to a stimulant challenge (Volkow et al.
2014c; van de Giessen et al.
2017).