ArticlePsychiatry and clinical neurosciences2020
Generation and analysis of novel Reln-deleted mouse model corresponding to exonic Reln deletion in schizophrenia.
Article in Psychiatry and clinical neurosciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
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- Regulatory mechanism of Reelin activity: a platform for exploiting Reelin as a therapeutic agent.Frontiers in molecular neuroscience · 2025Review
- Herbal Formula Extract Ameliorates Anxiety and Cognitive Impairment via Regulation of the Reelin/Dab-1 Pathway in a Murine Model of Post-Traumatic Stress Disorder.Pharmaceutics · 2024Article
- Mice with deficiency in Pcdh15, a gene associated with bipolar disorders, exhibit significantly elevated diurnal amplitudes of locomotion and body temperature.Translational psychiatry · 2024Article
- Phenotypes for general behavior, activity, and body temperature in 3q29 deletion model mice.Translational psychiatry · 2024Article
- Schizophrenia in the genetic era: a review from development history, clinical features and genomic research approaches to insights of susceptibility genes.Metabolic brain disease · 2024Review
- Reelin Signaling in Neurodevelopmental Disorders and Neurodegenerative Diseases.Brain sciences · 2023Review
- New Strategies for the Treatment of Neuropsychiatric Disorders Based on Reelin Dysfunction.International journal of molecular sciences · 2022Review
- The Pathophysiological Link Between Reelin and Autism: Overview and New Insights.Frontiers in genetics · 2022Review
- Trends in big data analyses by multicenter collaborative translational research in psychiatry.Psychiatry and clinical neurosciences · 2022Review
- Astrocyte Bioenergetics and Major Psychiatric Disorders.Advances in neurobiology · 2021Review
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
aimA Japanese individual with schizophrenia harboring a novel exonic deletion in RELN was recently identified by genome-wide copy-number variation analysis. Thus, the present study aimed to generate and analyze a model mouse to clarify whether Reln deficiency is associated with the pathogenesis of schizophrenia.
methodsA mouse line with a novel RELN exonic deletion (Reln-del) was established using the CRISPR/Cas9 method to elucidate the underlying molecular mechanism. Subsequently, general behavioral tests and histopathological examinations of the model mice were conducted and phenotypic analysis of the cerebellar granule cell migration was performed.
resultsThe phenotype of homozygous Reln-del mice was similar to that of reeler mice with cerebellar atrophy, dysplasia of the cerebral layers, and abrogated protein levels of cerebral reelin. The expression of reelin in heterozygous Reln-del mice was approximately half of that in wild-type mice. Conversely, behavioral analyses in heterozygous Reln-del mice without cerebellar atrophy or dysplasia showed abnormal social novelty in the three-chamber social interaction test. In vitro reaggregation formation and neuronal migration were severely altered in the cerebellar cultures of homozygous Reln-del mice.
conclusionThe present results in novel Reln-del mice modeled after our patient with a novel exonic deletion in RELN are expected to contribute to the development of reelin-based therapies for schizophrenia.
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