@alanajaskir.bsky.social @marcelomattar.bsky.social @nicoschuck.bsky.social @actlab.bsky.social

Thanks! Our technique is indirect (as, unlike PET, fMRI cannot directly assess dopamine), but it does seem to provide useful information linked to dopaminergic function.

thanks for sharing this!

Have you run your estimation on striatal subregions? I'd be very curious to see what the HRFs look like!

I’m curious to hear what you find! In the preprint, we don’t model the HRF directly, but we have a project looking into trial-by-trial variability in the NAcc HRF time-to-peak

Our TR was 2s. Would love to experiment with faster TRs in the future.

Check out our preprint to learn more about how hemodynamic latencies map regional, individual, and pathological differences linked to dopamine. We'd love to hear your questions, ideas, or feedback! @anneberry.bsky.social @blaisefrederick.bsky.social

In individuals with cocaine use disorder, we found a spatial gradient of altered hemodynamic latencies in the striatum. This pattern independently correlated with nicotine use, revealing a conserved physiological profile associated with addictive substance use. 5/n

Using PET, genetics, and pharmacology, we found that hemodynamic latency is tightly coupled to dopamine physiology. Broadly speaking, higher latency in the NAcc was associated with lower dopamine function and more perseverative behavior—linking BOLD signal timing to cognition. 4/n

Hemodynamic latencies are markedly increased in the nucleus accumbens (NAcc)—a key dopaminergic region linked to addiction. This effect is strikingly precise: the anatomical NAcc boundary (green) aligns closely with the shift in hemodynamic latency. 3/n

fMRI doesn’t directly measure dopamine, but could dopamine influence BOLD signal timing? Dopamine axons wrap around microvessels, and dopamine triggers vasoconstriction. We hypothesized that higher extracellular dopamine increases the latency of the hemodynamic response. 2/n