[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 compared with controls [40]. Because midbrain also includes the upper portion of the locus coeruleus, the main norepinephrinergic nucleus in the brain, and the upper part of the rostral raphe, which is the main source of serotonergic innervation to cerebellum and forebrain, and considering that the spatial resolution of fMRI is limited to few mm [41], altered functional connectivity of the midbrain with MDTHA, cerebellum, and rACC could reflect not just neuroadaptations in dopaminergic but also in norepinephrinergic and/or serotonergic neurotransmission with chronic cocaine exposure.
