cortex, putamen bilaterally and precuneus in chronic cannabis users. However, there were no significant differences between the groups in striatal D2/D3 receptor availability and no correlation between striatal [11C]-raclopride-PET binding potential and glucose metabolism [159]. Consistent with these results, three other [11C]- raclopride-PET studies [160]–[162] failed to find any differences between groups in dopamine D2/D3 receptor availability in the striatum as a whole or it functional subdivisions. However, while Stokes et al. (2012) [160] also failed to find any association between lifetime frequency of cannabis use and binding potential values, Albrecht et al. (2012) [161] described a negative correlation with both urine levels of cannabis metabolites and self-report of recent cannabis consumption. Finally, Hirvonen et al. (2011) [163] demonstrated a reversible and regionally selective downregulation of CB1 receptors. At baseline, current users had approximately 20% less CB1 receptor density in the neocortex and limbic regions, which was negatively correlated with years of cannabis exposure. After four weeks of abstinence from cannabis use, CB1 receptor density returned to normal levels in all brain regions, except for the hippocampus [163].
