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Loss of calsyntenin paralogs disrupts interneuron stability and mouse behavior
Bibliographic Information
- Published
- 2022-03-12
- Resource Type
- journal article
- Rights Information
-
- https://creativecommons.org/licenses/by/4.0
- https://creativecommons.org/licenses/by/4.0
- DOI
-
- 10.1186/s13041-022-00909-8
- Publisher
- Springer Science and Business Media LLC
Description
<jats:title>Abstract</jats:title><jats:p>Calsyntenins (CLSTNs) are important synaptic molecules whose molecular functions are not fully understood. Although mutations in <jats:italic>calsyntenin</jats:italic> (<jats:italic>CLSTN</jats:italic>) 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 <jats:italic>Clstn</jats:italic> 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.</jats:p>
Journal
-
- Molecular Brain
-
Molecular Brain 15 (1), 2022-03-12
Springer Science and Business Media LLC
