ArticlebioRxiv : the preprint server for biology2025
Schizophrenia-associated 22q11.2 deletion elevates striatal acetylcholine and disrupts thalamostriatal projections to produce amotivation in mice.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Schizophrenia is a complex neurodevelopmental disorder characterized by cognitive dysfunction, hallucinations, and negative symptoms such as amotivation. Negative symptoms are largely resistant to current antipsychotic treatments, and the neural circuits underlying amotivational states remain poorly defined. Here, using a mouse model of schizophrenia-associated 22q11.2 deletion syndrome (22q11DS), we report amotivation and weakened glutamatergic synaptic transmission between the thalamic parafascicular nucleus (Pf) and the dorsomedial striatum (DMS). Thalamostriatal disruption is attributed to hyperactivity of striatal cholinergic interneurons (CHIs), which is associated with enhanced
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