Impaired Axonal Na+ Current by Hindlimb Unloading : Implication for Disuse Neuromuscular Atrophy

• Material Type: 博士論文
• Title: Impaired Axonal Na+ Current by Hindlimb Unloading : Implication for Disuse Neuromuscular Atrophy
• Author/Editor: Banzrai, Chimeglkham; Nodera, Hiroyuki; Kawarai, Toshitaka; Higashi, Saki; Okada, Ryo; Mori, Atsuko; Shimatani, Yoshimitsu; Osaki, Yusuke; Kaji, Ryuji
• Author Heading: Banzrai, Chimeglkham; Nodera, Hiroyuki; Kawarai, Toshitaka; Higashi, Saki; Okada, Ryo; Mori, Atsuko; Shimatani, Yoshimitsu; Osaki, Yusuke; Kaji, Ryuji
• Publication, Distribution, etc.: Frontiers Media S.A.
• Publication Date: 2016-02-16
• Publication Date (W3CDTF): 2016-02-16
• Alternative Title: 尾懸垂による神経軸索Na+電流の障害 : 廃用性筋萎縮との関連の可能性; Sodium Current by Hindlimb Unloading
• Periodical title: Frontiers in Physiology
• No. or year of volume/issue: 7
• Volume: 7
• Pages: 36-
• ISSN (Periodical Title): ISSN : 1664-042X
• Degree grantor/type: 徳島大学
• Date Granted: 2016-03-23
• Dissertation Number: 甲第2959号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: Disuse neuromuscular atrophy; hindlimb-unloading; motor axonal excitability; sodium current; neural plasticity; axonal excitability; disuse atrophy; persistent sodium current; ion channels; hreshold tracking
• Target Audience: 一般
• Note (General): This study aimed to characterize the excitability changes in peripheral motor axons caused by hindlimb unloading (HLU), which is a model of disuse neuromuscular atrophy. HLU was performed in normal 8-week-old male mice by fixing the proximal tail by a clip connected to the top of the animal's cage for 3 weeks. Axonal excitability studies were performed by stimulating the sciatic nerve at the ankle and recording the compound muscle action potential (CMAP) from the foot. The amplitudes of the motor responses of the unloading group were 51% of the control amplitudes [2.2 ± 1.3 mV (HLU) vs. 4.3 ± 1.2 mV (Control), P = 0.03]. Multiple axonal excitability analysis showed that the unloading group had a smaller strength-duration time constant (SDTC) and late subexcitability (recovery cycle) than the controls [0.075 ± 0.01 (HLU) vs. 0.12 ± 0.01 (Control), P < 0.01; 5.4 ± 1.0 (HLU) vs. 10.0 ± 1.3 % (Control), P = 0.01, respectively]. Three weeks after releasing from HLU, the SDTC became comparable to the control range. Using a modeling study, the observed differences in the waveforms could be explained by reduced persistent Na+ currents along with parameters related to current leakage. Quantification of RNA of a SCA1A gene coding a voltage-gated Na+ channel tended to be decreased in the sciatic nerve in HLU. The present study suggested that axonal ion currents are altered in vivo by HLU. It is still undetermined whether the dysfunctional axonal ion currents have any pathogenicity on neuromuscular atrophy or are the results of neural plasticity by atrophy.
• Format (IMT): application/pdf
• Access Restrictions: インターネット公開
• Rights (production): Copyright: © 2016 Banzrai, Nodera, Kawarai, Higashi, Okada, Mori, Shimatani, Osaki and Kaji. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
• Related Material (DOI): 10.3389/fphys.2016.00036
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 徳島大学 : 徳島大学機関リポジトリ

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