Striatal dopamine mediates hallucination-like perception in mice
A computational model is devised that explains the emergence of hallucination-like percepts as a consequence of faulty perceptual inference when prior expectations outweigh sensory evidence and can serve as a translational model of psychotic symptoms.
Abstract
<jats:title>How to model hallucinations in mice</jats:title> <jats:p> There has not been enough progress in our understanding of the basic mechanisms underlying psychosis. Studying psychotic disorders in animal models is difficult because the diagnosis relies on self-reported symptoms that can only be assessed in humans. Schmack <jats:italic>et al.</jats:italic> developed a paradigm to probe and rigorously measure experimentally controlled hallucinations in rodents (see the Perspective by Matamales). Using dopamine-sensor measurements and circuit and pharmacological manipulations, they demonstrated a brain circuit link between excessive dopamine and hallucination-like experience. This could potentially be useful as a translational model of common psychotic symptoms described in various psychiatric disorders. It may also help in the development of new therapeutic approaches based on anatomically selective modulation of dopamine function. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.abf4740">eabf4740</jats:related-article> ; see also p. <jats:related-article issue="6537" page="33" related-article-type="in-this-issue" vol="372">33</jats:related-article> </jats:p>