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  1. C100 医学部/医学系研究科
  2. C100a 雑誌掲載論文
  3. 学術雑誌

Role of the BDNF-TrkB pathway in KCC2 regulation and rehabilitation following neuronal injury: A mini review

http://hdl.handle.net/2237/00030884
a1497c6a-924b-480f-a19e-2e266b83d8db
名前 / ファイル ライセンス アクション
reviewed reviewed paper_190301 (5.0 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2019-11-14
タイトル
タイトル Role of the BDNF-TrkB pathway in KCC2 regulation and rehabilitation following neuronal injury: A mini review
著者 Lee-Hotta, Sachiko

× Lee-Hotta, Sachiko

WEKO 94192

Lee-Hotta, Sachiko

Search repository
Uchiyama, Yasushi

× Uchiyama, Yasushi

WEKO 94193

Uchiyama, Yasushi

Search repository
Kametaka, Satoshi

× Kametaka, Satoshi

WEKO 94194

Kametaka, Satoshi

Search repository
権利
権利情報 © 2019. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
キーワード
主題Scheme Other
主題 BDNF-TrkB pathway
キーワード
主題Scheme Other
主題 KCC2
キーワード
主題Scheme Other
主題 Spasticity
キーワード
主題Scheme Other
主題 Spinal cord injury
抄録
内容記述 In most mature neurons, low levels of intracellular Cl− concentrations ([Cl−]i) are maintained by channels and transporters, particularly the K+-Cl- cotransporter 2 (KCC2), which is the only Cl− extruder in most neurons. Recent studies have implicated KCC2 expression in the molecular mechanisms underlying neuronal disorders, such as spasticity, epilepsy and neuropathic pain. Alterations in KCC2 expression have been associated with brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB). The present review summarizes recent progress regarding the roles of Cl− regulators in immature and mature neurons. Moreover, we focus on the role of KCC2 regulation via the BDNF-TrkB pathway in spinal cord injury and rehabilitation, as prior studies have shown that the BDNF-TrkB pathway can affect both the pathological development and functional amelioration of spinal cord injuries. Evidence suggests that rehabilitation using active exercise and mechanical stimulation can attenuate spasticity and neuropathic pain in animal models, likely due to the upregulation of KCC2 expression via the BDNF-TrkB pathway. Moreover, research suggests that such rehabilitation efforts may recover KCC2 expression without the use of exogenous BDNF.
内容記述タイプ Abstract
内容記述
内容記述 ファイル公開:2020-09-01
内容記述タイプ Other
出版者
出版者 Elsevier
言語
言語 eng
資源タイプ
資源タイプresource http://purl.org/coar/resource_type/c_6501
タイプ journal article
DOI
関連識別子
識別子タイプ DOI
関連識別子 https://doi.org/10.1016/j.neuint.2019.04.003
ISSN(print)
収録物識別子タイプ ISSN
収録物識別子 0197-0186
書誌情報 Neurochemistry International

巻 128, p. 32-38, 発行日 2019-09
著者版フラグ
値 author
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