Impairment of social behaviors in Arhgef10 knockout mice
| العنوان: | Impairment of social behaviors in Arhgef10 knockout mice |
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| المؤلفون: | Chia-Hsiang Chen, Susan Shur-Fen Gau, Dai-Hua Lu, Houng-Chi Liou, Huang-Ju Tu, Hsiao-Mei Liao, Wen-Mei Fu |
| المصدر: | Molecular Autism Molecular Autism, Vol 9, Iss 1, Pp 1-14 (2018) |
| بيانات النشر: | BioMed Central, 2018. |
| سنة النشر: | 2018 |
| مصطلحات موضوعية: | 0301 basic medicine, Male, medicine.medical_specialty, Serotonin, Autism Spectrum Disorder, Morris water navigation task, lcsh:RC346-429, 03 medical and health sciences, Norepinephrine, Mice, 0302 clinical medicine, Developmental Neuroscience, Dopamine, Internal medicine, medicine, Animals, Learning, Social Behavior, Molecular Biology, Monoamine Oxidase, lcsh:Neurology. Diseases of the nervous system, biology, business.industry, Research, Institutional Animal Care and Use Committee, Brain, medicine.disease, Mice, Inbred C57BL, Psychiatry and Mental health, 030104 developmental biology, Endocrinology, Autism spectrum disorder, Social deficits, Knockout mouse, biology.protein, Monoamine oxidase A, ARHGEF10, business, 030217 neurology & neurosurgery, Rho Guanine Nucleotide Exchange Factors, Developmental Biology, Social behavior, medicine.drug |
| الوصف: | Background Impaired social interaction is one of the essential features of autism spectrum disorder (ASD). Our previous copy number variation (CNV) study discovered a novel deleted region associated with ASD. One of the genes included in the deleted region is ARHGEF10. A missense mutation of ARHGEF10 has been reported to be one of the contributing factors in several diseases of the central nervous system. However, the relationship between the loss of ARHGEF10 and the clinical symptoms of ASD is unclear. Methods We generated Arhgef10 knockout mice as a model of ASD and characterized the social behavior and the biochemical changes in the brains of the knockout mice. Results Compared with their wild-type littermates, the Arhgef10-depleted mice showed social interaction impairment, hyperactivity, and decreased depression-like and anxiety-like behavior. Behavioral measures of learning in the Morris water maze were not affected by Arhgef10 deficiency. Moreover, neurotransmitters including serotonin, norepinephrine, and dopamine were significantly increased in different brain regions of the Arhgef10 knockout mice. In addition, monoamine oxidase A (MAO-A) decreased in several brain regions. Conclusions These results suggest that ARHGEF10 is a candidate risk gene for ASD and that the Arhgef10 knockout model could be a tool for studying the mechanisms of neurotransmission in ASD. Trial registration Animal studies were approved by the Institutional Animal Care and Use Committee of National Taiwan University (IACUC 20150023). Registered 1 August 2015. Electronic supplementary material The online version of this article (10.1186/s13229-018-0197-5) contains supplementary material, which is available to authorized users. |
| اللغة: | English |
| تدمد: | 2040-2392 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c72473a4cf2d9162dbf45b695dd39172 http://europepmc.org/articles/PMC5810065 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....c72473a4cf2d9162dbf45b695dd39172 |
| قاعدة البيانات: | OpenAIRE |
Find this article in full text from Springer Verlag. | تدمد: | 20402392 |
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