A corticostriatal learning mechanism linking excess striatal dopamine and auditory hallucinations.

Auditory hallucinations are linked to elevated striatal dopamine, but their underlying computational mechanisms have been obscured by regional heterogeneity in striatal dopamine signaling. To address this, we developed a normative circuit model in which corticostriatal plasticity in the ventral striatum is modulated by reward prediction errors to drive reinforcement learning while that in the sensory-dorsal striatum is modulated by sensory prediction errors derived from internal belief to drive self-supervised learning. We then validate the key predictions of this model using dopamine recordings across striatal regions in mice, as well as human behavior in a hybrid learning task. Finally, we find that changes in learning resulting from optogenetic stimulation of the sensory striatum in mice and individual variability in hallucination proneness in humans are best explained by selectively enhancing dopamine levels in the model sensory striatum. These findings identify plasticity mechanisms underlying biased learning of sensory expectations as a biologically plausible link between excess dopamine and hallucinations.