The neurobiological mechanisms that underlie dopamine-dependent auditory hallucinatory states, with therapeutic implications, are uncovered by Schmack et al. (5).
An increase of dopamine in the striatum virtualizes a nonexistent auditory signal in mice The ability to detect external stimuli rapidly and accurately by building internal sensory representations is a central computation of the brain that is critical to guide behavior. Such expectations (or priors) may be acquired throughout the lifetime of an individual and are important to influence perception, particularly when incoming sensory signals are ambiguous (1). But this process is not exempt from failure. Hallucinations (perceptual experiences without external stimuli) seen in conditions such as schizophrenia are thought to result from giving too much weight to priors, creating an imbalance at the expense of actual sensory evidence (2, 3). Sustained high-dopamine tone in the striatum has been proposed to contribute to this imbalance (4); however, it has remained unclear how the dopaminergic perturbation leads to the generation of hallucinations. On page 51 of this issue, Schmack et al. (5) uncover the neurobiological mechanisms that underlie dopamine-dependent auditory hallucinatory states, with therapeutic implications.