| First Author | Nomiya H | Year | 2024 |
| Journal | Sci Rep | Volume | 14 |
| Issue | 1 | Pages | 3376 |
| PubMed ID | 38336912 | Mgi Jnum | J:347274 |
| Mgi Id | MGI:7595025 | Doi | 10.1038/s41598-024-53237-3 |
| Citation | Nomiya H, et al. (2024) A Kpna1-deficient psychotropic drug-induced schizophrenia model mouse for studying gene-environment interactions. Sci Rep 14(1):3376 |
| abstractText | KPNA1 is a mediator of nucleocytoplasmic transport that is abundantly expressed in the mammalian brain and regulates neuronal differentiation and synaptic function. De novo mutations in Kpna1 have been identified using genome-wide association studies in humans with schizophrenia; however, it remains unclear how KPNA1 contributes to schizophrenia pathogenesis. Recent studies have suggested a complex combination of genetic and environmental factors that are closely related to psychiatric disorders. Here, we found that subchronic administration of phencyclidine, a psychotropic drug, induced vulnerability and behavioral abnormalities consistent with the symptoms of schizophrenia in Kpna1-deficient mice. Microarray assessment revealed that the expression levels of dopamine d1/d2 receptors, an RNA editing enzyme, and a cytoplasmic dynein component were significantly altered in the nucleus accumbens brain region in a gene-environment (G x E) interaction-dependent manner. Our findings demonstrate that Kpna1-deficient mice may be useful as a G x E interaction mouse model for psychiatric disorders and for further investigation into the pathogenesis of such diseases and disorders. |
