Hallucinations, a central symptom of psychotic disorders, are attributed to excessive dopamine in the brain. However, the neural circuit mechanisms by which dopamine produces hallucinations remain elusive, largely because hallucinations have been challenging to study in model organisms. We developed a task to quantify hallucination-like perception in mice. Hallucination-like percepts, defined as high-confidence false detections, increased after hallucination-related manipulations in mice and correlated with self-reported hallucinations in humans. Hallucination-like percepts were preceded by elevated striatal dopamine levels, could be induced by optogenetic stimulation of mesostriatal dopamine neurons, and could be reversed by the antipsychotic drug haloperidol. These findings reveal a causal role for dopamine-dependent striatal circuits in hallucination-like perception and open new avenues to develop circuit-based treatments for psychotic disorders.

幻觉是精神病的主要症状，归因于大脑中的多巴胺过多。然而，多巴胺产生幻觉的神经回路机制仍然难以捉摸，这主要是因为幻觉一直难以在模型生物中进行研究。我们开发了一项任务，以量化小鼠中的幻觉样感觉。幻觉样感知被定义为高可信度的虚假检测，在小鼠进行幻觉相关操作后增加，并与人类自我报告的幻觉相关。幻觉样感觉之前，纹状体多巴胺水平升高，可通过光遗传学刺激间皮多巴胺神经元来诱导，并可被抗精神病药氟哌啶醇逆转。