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Intracellular Cl? dysregulation causing and caused by pathogenic neuronal activity
http://hdl.handle.net/10271/00003774
http://hdl.handle.net/10271/00003774fedb3424-13a1-4a6e-89bb-3549f577082b
名前 / ファイル | ライセンス | アクション |
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Item type | 学術雑誌論文 / Journal Article(1) | |||||||||
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公開日 | 2021-04-26 | |||||||||
タイトル | ||||||||||
タイトル | Intracellular Cl? dysregulation causing and caused by pathogenic neuronal activity | |||||||||
言語 | en | |||||||||
言語 | ||||||||||
言語 | eng | |||||||||
キーワード | ||||||||||
主題 | Cl? homeostasis | |||||||||
キーワード | ||||||||||
主題 | KCC2 | |||||||||
キーワード | ||||||||||
主題 | GABAA receptor | |||||||||
キーワード | ||||||||||
主題 | Cl? channel | |||||||||
キーワード | ||||||||||
主題 | epilepsy | |||||||||
資源タイプ | ||||||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
資源タイプ | journal article | |||||||||
著者 |
Akita, Tenpei
× Akita, Tenpei
× Fukuda, Atsuo
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書誌情報 |
Pflu?gers Archiv : European journal of physiology 巻 472, 号 7, p. 977-987, 発行日 2020-07 |
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出版者 | ||||||||||
出版者 | Springer Nature | |||||||||
権利 | ||||||||||
権利情報 | "This is a post-peer-review, pre-copyedit version of an article published in ""Pflu?gers Archiv : European journal of physiology"". The final authenticated version is available online at: https://doi.org/10.1016/j.lungcan.2020.03.013" | |||||||||
抄録 | ||||||||||
内容記述タイプ | Abstract | |||||||||
内容記述 | The intracellular Cl? concentration ([Cl?]i) is tightly regulated in brain neurons for stabilizing brain performance. The [Cl?]i in mature neurons is determined by the balance between the rate of Cl? extrusion mainly mediated by the neuron-specific type 2 K?-Cl? cotransporter (KCC2) and the rate of Cl? entry through various Cl? channels including GABAA receptors during neuronal activity. Disturbance of the balance causes instability of brain circuit performance and may lead to epileptic seizures. In the first part of this review, we discuss how genetic alterations in KCC2 in humans cause infantile migrating focal seizures, based on our previous report and others. Depolarization of the membrane potential increases the driving force for Cl? entry into neurons. Thus, the duration of action potential spike generation and the frequency of excitatory synaptic inputs are the crucial factors for determining the total amount of Cl? entry and the equilibrium [Cl?]i in neurons. Moreover, there is also a significant interdependence between the neuronal activity and the KCC2 expression. In the second part, we discuss plausible mechanisms by which excessive neuronal activity due to excitotoxic brain insults or other epilepsy-associated gene mutations may cause the Cl? imbalance in neurons and lead to epileptic discharges over the brain, using the schematic “unifying foci” model based on literature. | |||||||||
ISSN | ||||||||||
収録物識別子タイプ | ISSN | |||||||||
収録物識別子 | 0031-6768 | |||||||||
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収録物識別子タイプ | ISSN | |||||||||
収録物識別子 | 1432-2013 | |||||||||
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関連タイプ | isVersionOf | |||||||||
識別子タイプ | PMID | |||||||||
関連識別子 | 32300887 | |||||||||
出版社DOI | ||||||||||
関連タイプ | isVersionOf | |||||||||
識別子タイプ | DOI | |||||||||
関連識別子 | 10.1007/s00424-020-02375-4 | |||||||||
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出版タイプ | AM | |||||||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa |