To indirectly assess if the low D2 receptor availability was due to lower D2 receptors levels and not higher D2 receptor occupancy by dopamine, we measured the correlation (Pearson’s product-moment) between D2 receptor availability and the changes in [11C]raclopride binding induced by 0.5 mg/kg of intravenous methylphenidate, which we had previously determined in these subjects (3). Because methylphenidate increases dopamine levels by blocking dopamine transporters (not by dopamine release) (4), the accumulation is a function of the amount of dopamine released at baseline, and hence the measure of methylphenidate-induced dopamine changes can be used as an indicator of baseline dopamine release. Measures of D2 receptor availability were significantly correlated with the changes in raclopride binding (baseline minus methylphenidate) (r=0.55, df=22, p<0.007). The lower the D2 receptor availability at baseline, the lower the dopamine changes, and vice versa. This is a strong indication that subjects with low D2 receptor availability did not have enhanced synaptic dopamine (and thus enhanced D2 receptor occupancy by dopamine) and those with high D2 receptor availability did not have decreased dopamine release (and decreased D2 receptor occupancy). Therefore, these results suggest that the differences in D2 receptor availability reflect differences in D2 receptor levels and support the involvement of D2 receptors as one of the molecular targets that modulates vulnerability to drug addiction.