ArticleNature communications2024
Synaptotagmin-11 deficiency mediates schizophrenia-like behaviors in mice via dopamine over-transmission.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Parallel anterior cingulate cortex pathways underlie dissociable social and attentional outputs.Science advances · 2026Article
- Hippocampal small RNAs from patients with schizophrenia induce specific cognitive and neural phenotypes in mice.Cell death discovery · 2026Article
- Derivatization-assisted dual-mode colorimetric and fluorometric detection of dopamine using 4-hexyl resorcinol.RSC advances · 2026Article
- Selective magnetic stimulation downregulates the GABAMolecular psychiatry · 2026Article
- Central neural circuits and their associated mechanisms of inter-organ crosstalk.Frontiers in cell and developmental biology · 2026Review
- Calcium-sensitive synaptotagmin 11-lipid interaction modulates exo-endocytosis.Nature communications · 2025Article
- A proteomic signature of vascular dysfunction linked to tauopathy and degeneration in the aging brain.bioRxiv : the preprint server for biology · 2025Article
- Remolding laccase for whole-cell and in vivo modulation of dopamine signal.Science advances · 2025Article
- CaNeuromolecular medicine · 2025Article
- Brain circuits that regulate social behavior.Molecular psychiatry · 2025Review
- Human Midbrain Organoids Enriched With Dopaminergic Neurons for Long-Term Functional Evaluation.Cell proliferation · 2025Article
- Electrochemical Sensor Capable of Enhancing Dopamine Sensitivity Based on Micron-Sized Metal-Organic Frameworks.Biosensors · 2025Article
- Action Potential Firing Patterns Regulate Dopamine Release via Voltage-Sensitive Dopamine D2 Autoreceptors in Mouse Striatum In Vivo.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
34 authors.
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Abstract
Schizophrenia is a severe neuropsychiatric disease, but the initiation mechanisms are unclear. Although antipsychotics are effective against positive symptoms, therapeutic interventions for negative symptoms are limited due to the lack of pathophysiological mechanisms. Here we identify synaptotagmin-11 (Syt11) as a potential genetic risk factor and dopamine over-transmission as a mechanism in the development of schizophrenia. Syt11 expression is reduced in individuals with schizophrenia but restored following the treatment with antipsychotics. Syt11 deficiency in dopamine neurons in early adolescence, but not in adults, leads to persistent social deficits and other schizophrenia-like behaviors by mediating dopamine over-transmission in mice. Accordingly, dopamine neuron over-excitation before late adolescence induces persistent schizophrenia-associated behavioral deficits, along with the structural and functional alternations in the mPFC. Notably, local intervention of D2R with clinical drugs presynaptically or postsynaptically exhibits both acute and long-lasting therapeutic effects on social deficits in schizophrenia mice models. These findings not only define Syt11 as a risk factor and DA over-transmission as a potential risk factor initiating schizophrenia, but also propose two D2R-targeting strategies for the comprehensive and long-term recovery of schizophrenia-associated social withdrawal.
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