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

DOI 機関リポジトリ NDLデジタルコレクション

書誌事項

タイトル
Impaired Axonal Na+ Current by Hindlimb Unloading : Implication for Disuse Neuromuscular Atrophy
タイトル別名
  • 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
著者
バンズライ, チメグルハム
著者別名
  • Banzrai, Chimeglkham
著者
野寺, 裕之
著者別名
  • ノデラ, ヒロユキ
  • Nodera, Hiroyuki
著者
瓦井, 俊孝
著者別名
  • カワライ, トシタカ
  • Kawarai, Toshitaka
著者
ヒガシ, サキ
著者別名
  • Higashi, Saki
著者
オカダ, リョウ
著者別名
  • Okada, Ryo
著者
モリ, アツコ
著者別名
  • Mori, Atsuko
著者
島谷, 佳光
著者別名
  • シマタニ, ヨシミツ
  • Shimatani, Yoshimitsu
著者
大崎, 裕亮
著者別名
  • オオサキ, ユウスケ
  • Osaki, Yusuke
著者
梶, 龍兒
著者別名
  • カジ, リュウジ
  • Kaji, Ryuji
学位授与大学
徳島大学
取得学位
博士（医学）
学位授与番号
甲医第1292号
学位授与年月日
2016-03-23

説明

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.

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