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題名 Loss of CDKL5 disrupts respiratory function in mice
作者 廖文霖
Lee, Kun-Ze
Liao, Wenlin
貢獻者 神經科學研究所
關鍵詞 CDKL5; Respiration; Tidal volume; Hypoxia; Hypercapnia
日期 2018-01
上傳時間 29-Jan-2018 10:45:27 (UTC+8)
摘要 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.
關聯 Respiratory Physiology & Neurobiology, Volume 248, Pages 48-54
資料類型 article
DOI https://doi.org/10.1016/j.resp.2017.11.010
dc.contributor 神經科學研究所
dc.creator (作者) 廖文霖zh_TW
dc.creator (作者) Lee, Kun-Zeen_US
dc.creator (作者) Liao, Wenlinen_US
dc.date (日期) 2018-01
dc.date.accessioned 29-Jan-2018 10:45:27 (UTC+8)-
dc.date.available 29-Jan-2018 10:45:27 (UTC+8)-
dc.date.issued (上傳時間) 29-Jan-2018 10:45:27 (UTC+8)-
dc.identifier.uri (URI) http://nccur.lib.nccu.edu.tw/handle/140.119/115630-
dc.description.abstract (摘要) 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.en_US
dc.format.extent 1047316 bytes-
dc.format.mimetype application/pdf-
dc.relation (關聯) Respiratory Physiology & Neurobiology, Volume 248, Pages 48-54
dc.subject (關鍵詞) CDKL5; Respiration; Tidal volume; Hypoxia; Hypercapniaen_US
dc.title (題名) Loss of CDKL5 disrupts respiratory function in miceen_US
dc.type (資料類型) article
dc.identifier.doi (DOI) 10.1016/j.resp.2017.11.010
dc.doi.uri (DOI) https://doi.org/10.1016/j.resp.2017.11.010