Academic Journal

Dyslexia‐Related Hearing Loss Occurs Mainly through the Abnormal Spontaneous Electrical Activity of Spiral Ganglion Neurons

التفاصيل البيبلوغرافية
العنوان: Dyslexia‐Related Hearing Loss Occurs Mainly through the Abnormal Spontaneous Electrical Activity of Spiral Ganglion Neurons
المؤلفون: Guodong Hong, Xiaolong Fu, Xin Chen, Liyan Zhang, Xuan Han, Shuqin Ding, Ziyi Liu, Xiuli Bi, Wen Li, Miao Chang, Ruifeng Qiao, Siwei Guo, Hailong Tu, Renjie Chai
المصدر: Advanced Science, Vol 10, Iss 16, Pp n/a-n/a (2023)
بيانات النشر: Wiley, 2023.
سنة النشر: 2023
المجموعة: LCC:Science
مصطلحات موضوعية: Dyslexia, Dyx1c1, hearing loss, neurodevelopmental disorder, Science
الوصف: Abstract Dyslexia is a reading and spelling disorder due to neurodevelopmental abnormalities and is occasionally found to be accompanied by hearing loss, but the reason for the associated deafness remains unclear. This study finds that knockout of the dyslexia susceptibility 1 candidate 1 gene (Dyx1c1−/−) in mice, the best gene for studying dyslexia, causes severe hearing loss, and thus it is a good model for studying the mechanism of dyslexia‐related hearing loss (DRHL). This work finds that the Dyx1c1 gene is highly expressed in the mouse cochlea and that the spontaneous electrical activity of inner hair cells and type I spiral ganglion neurons is altered in the cochleae of Dyx1c1−/− mice. In addition, primary ciliary dyskinesia‐related phenotypes such as situs inversus and disrupted ciliary structure are seen in Dyx1c1−/− mice. In conclusion, this study gives new insights into the mechanism of DRHL in detail and suggests that Dyx1c1 may serve as a potential target for the clinical diagnosis of DRHL.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2198-3844
Relation: https://doaj.org/toc/2198-3844
DOI: 10.1002/advs.202205754
URL الوصول: https://doaj.org/article/f1bbf585e60f417d8bb6c0a72d6cba50
رقم الانضمام: edsdoj.f1bbf585e60f417d8bb6c0a72d6cba50
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:21983844
DOI:10.1002/advs.202205754