Abstract
Spatial variations in dopamine function are linked to cognition and substance use disorders but are challenging to characterize with current methods. Because dopamine influences blood vessel dilation, we hypothesized that hemodynamic latency, which reflects BOLD signal timing, could serve as an indirect marker of dopamine physiology. Across four datasets, we found a topography of hemodynamic latencies that precisely distinguished the nucleus accumbens, a dopaminergic region implicated in motivation and substance abuse, from other striatal regions. Using PET, genetics, and pharmacology, we found that hemodynamic latencies are robustly related to dopamine function and dopamine-linked behavior. In individuals with cocaine use disorder, we observed a spatial gradient of altered hemodynamic latencies in the striatum. This pattern independently predicted nicotine use, revealing a conserved physiological profile associated with addictive substance use. Hemodynamic latencies map regional, individual, and pathological differences linked to dopamine, opening new avenues for indirectly assessing the role of dopamine in healthy cognition and disease.