ArticleMolecular brain2022
Loss of calsyntenin paralogs disrupts interneuron stability and mouse behavior.
Article in Molecular brain, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 16 citations in OpenAlex.
- Neuromodulation of swarming behavior inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Neuromodulation of Swarming Behavior inbioRxiv : the preprint server for biology · 2025Article
- Genome-wide association of tau neuroimaging and plasma biomarkers in adults with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Genome-wide identification and spatiotemporal expression analysis of cadherin superfamily members in echinoderms.EvoDevo · 2023Article
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Authors and funding
9 authors at 4 institutions in 1 country.
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Abstract
Calsyntenins (CLSTNs) are important synaptic molecules whose molecular functions are not fully understood. Although mutations in calsyntenin (CLSTN) genes have been associated with psychiatric disorders in humans, their function is still unclear. One of the reasons why the function of CLSTNs in the nervous system has not been clarified is the functional redundancy among the three paralogs. Therefore, to investigate the functions of mammalian CLSTNs, we generated triple knockout (TKO) mice lacking all CLSTN paralogs and examined their behavior. The mutant mice tended to freeze in novel environments and exhibited hypersensitivity to stress. Consistent with this, glucose levels under stress were significantly higher in the mutant mice than in the wild-type controls. In particular, phenotypes such as decreased motivation, which had not been reported in single Clstn KO mice, were newly discovered. The TKO mice generated in this study represent an important mouse model for clarifying the function of CLSTN in the future.
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