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政大機構典藏 > 理學院 > 神經科學研究所 > 期刊論文 > Item 140.119/115630

Please use this identifier to cite or link to this item: https://nccur.lib.nccu.edu.tw/handle/140.119/115630

Title:	Loss of CDKL5 disrupts respiratory function in mice
Authors:	廖文霖 Lee, Kun-Ze Liao, Wenlin
Contributors:	神經科學研究所
Keywords:	CDKL5;Respiration;Tidal volume;Hypoxia;Hypercapnia
Date:	2018-01
Issue Date:	2018-01-29 10:45:27 (UTC+8)
Abstract:	Cyclin-dependent kinase-like 5 (CDKL5) is an X-linked gene encoding a serine-threonine kinase that is highly expressed in the central nervous system. Mutations in CDKL5 cause neurological and psychiatric symptoms, including early-onset seizures, motor dysfunction, autistic features and sleep breathing abnormalities in patients. It remains to be addressed whether loss of CDKL5 causes respiratory dysfunction in mice. Here, we examined the respiratory pattern of male Cdkl5−/y mice at 1–3 months of age during resting breathing and respiratory challenge (i.e., hypoxia and hypercapnia) via whole body plethysmography. The results demonstrated that the resting respiratory frequency and tidal volume of Cdkl5−/y mice was unaltered compared to that of WT mice at 1 month of age. However, these mutant mice exhibit transient reduction in tidal volume during respiratory challenge even the reduction was restored at 2 months of age. Notably, the sigh-breathing pattern was changed in Cdkl5−/y mice, showing a transient reduction in sigh volume at 1–2 month of age and long-term attenuation of peak expiratory airflow from 1 to 3 month of age. Therefore, loss of CDKL5 causes breathing deficiency, supporting a CDKL5-mediated regulation of respiratory function in mice.
Relation:	Respiratory Physiology & Neurobiology, Volume 248, Pages 48-54
Data Type:	article
DOI 連結:	https://doi.org/10.1016/j.resp.2017.11.010
DOI:	10.1016/j.resp.2017.11.010
Appears in Collections:	[神經科學研究所 ] 期刊論文

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