Using the DW task we recently showed that drug words, but not neutral words, activated the midbrain in cocaine subjects but not in controls [15]. In the current work we evaluated the functional connectivity of this midbrain region (Talairach coordinates xyz = [−6, −15, −18] mm) with the rest of the brain using a different sample and a simplified version of the stimulation paradigm. Since the midbrain is relatively small and the imaging smoothing was larger than 12-mm is all directions, the functional responses in the selected seed region are representative of those in the entire midbrain. The midbrain (mesencephalon) is the origin of the main dopamine (DA) projections to the forebrain, and cocaine addicts have lower dopaminergic function than controls [5]. Since cocaine binds to norepinephrine (NE) and DA transporters [37], thereby increasing extracellular NE and DA [1], [38], [39], chronic cocaine exposure could be additionally associated with disrupted neurotransmission in noradrenergic pathways including those into the thalamus. Indeed recent imaging studies have provided evidence of noradrenergic abnormalities in the thalamus (including medial dorsal nuclei) of cocaine abusers when
