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

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Bibliographic Information

Title
Impaired Axonal Na+ Current by Hindlimb Unloading : Implication for Disuse Neuromuscular Atrophy
Other 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
Author
Banzrai, Chimeglkham
Alias Name
  • バンズライ, チメグルハム
  • バンズライ, チメグルハム
Author
Nodera, Hiroyuki
Alias Name
  • 野寺, 裕之
  • ノデラ, ヒロユキ
Author
Kawarai, Toshitaka
Alias Name
  • 瓦井, 俊孝
  • カワライ, トシタカ
Author
Higashi, Saki
Alias Name
  • ヒガシ, サキ
  • ヒガシ, サキ
Author
Okada, Ryo
Alias Name
  • オカダ, リョウ
  • オカダ, リョウ
Author
Mori, Atsuko
Alias Name
  • モリ, アツコ
  • モリ, アツコ
Author
Shimatani, Yoshimitsu
Alias Name
  • 島谷, 佳光
  • シマタニ, ヨシミツ
Author
Osaki, Yusuke
Alias Name
  • 大崎, 裕亮
  • オオサキ, ユウスケ
Author
Kaji, Ryuji
Alias Name
  • 梶, 龍兒
  • カジ, リュウジ
University
徳島大学
Types of degree
博士（医学）
Grant ID
甲医第1292号
Degree year
2016-03-23

Description

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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