Molecular Mechanisms of Treadmill Therapy on Neuromuscular Atrophy Induced via Botulinum Toxin A
Botulinum toxin A (BoNT-A) is a bacterial zinc-dependent endopeptidase that acts specifically on neuromuscular junctions. BoNT-A blocks the release of acetylcholine, thereby decreasing the ability of a spastic muscle to generate forceful contraction, which results in a temporal local weakness and th...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2013/593271 |
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| author | Sen-Wei Tsai Hsiao-Ling Chen Yi-Chun Chang Chuan-Mu Chen |
| author_facet | Sen-Wei Tsai Hsiao-Ling Chen Yi-Chun Chang Chuan-Mu Chen |
| author_sort | Sen-Wei Tsai |
| collection | DOAJ |
| description | Botulinum toxin A (BoNT-A) is a bacterial zinc-dependent endopeptidase that acts specifically on neuromuscular junctions. BoNT-A blocks the release of acetylcholine, thereby decreasing the ability of a spastic muscle to generate forceful contraction, which results in a temporal local weakness and the atrophy of targeted muscles. BoNT-A-induced temporal muscle weakness has been used to manage skeletal muscle spasticity, such as poststroke spasticity, cerebral palsy, and cervical dystonia. However, the combined effect of treadmill exercise and BoNT-A treatment is not well understood. We previously demonstrated that for rats, following BoNT-A injection in the gastrocnemius muscle, treadmill running improved the recovery of the sciatic functional index (SFI), muscle contraction strength, and compound muscle action potential (CMAP) amplitude and area. Treadmill training had no influence on gastrocnemius mass that received BoNT-A injection, but it improved the maximal contraction force of the gastrocnemius, and upregulation of GAP-43, IGF-1, Myo-D, Myf-5, myogenin, and acetylcholine receptor (AChR) subunits α and β was found following treadmill training. Taken together, these results suggest that the upregulation of genes associated with neurite and AChR regeneration following treadmill training may contribute to enhanced gastrocnemius strength recovery following BoNT-A injection. |
| format | Article |
| id | doaj-art-cc31f8cb7bd74f179e533ba5bb1fe5cc |
| institution | OA Journals |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-cc31f8cb7bd74f179e533ba5bb1fe5cc2025-08-20T02:19:57ZengWileyNeural Plasticity2090-59041687-54432013-01-01201310.1155/2013/593271593271Molecular Mechanisms of Treadmill Therapy on Neuromuscular Atrophy Induced via Botulinum Toxin ASen-Wei Tsai0Hsiao-Ling Chen1Yi-Chun Chang2Chuan-Mu Chen3Department of Life Sciences, Agricultural Biotechnology Center, National Chung Hsing University, Taichung 402, TaiwanDepartment of Bioresources, Da-Yeh University, Changhua 515, TaiwanDepartment of Life Sciences, Agricultural Biotechnology Center, National Chung Hsing University, Taichung 402, TaiwanDepartment of Life Sciences, Agricultural Biotechnology Center, National Chung Hsing University, Taichung 402, TaiwanBotulinum toxin A (BoNT-A) is a bacterial zinc-dependent endopeptidase that acts specifically on neuromuscular junctions. BoNT-A blocks the release of acetylcholine, thereby decreasing the ability of a spastic muscle to generate forceful contraction, which results in a temporal local weakness and the atrophy of targeted muscles. BoNT-A-induced temporal muscle weakness has been used to manage skeletal muscle spasticity, such as poststroke spasticity, cerebral palsy, and cervical dystonia. However, the combined effect of treadmill exercise and BoNT-A treatment is not well understood. We previously demonstrated that for rats, following BoNT-A injection in the gastrocnemius muscle, treadmill running improved the recovery of the sciatic functional index (SFI), muscle contraction strength, and compound muscle action potential (CMAP) amplitude and area. Treadmill training had no influence on gastrocnemius mass that received BoNT-A injection, but it improved the maximal contraction force of the gastrocnemius, and upregulation of GAP-43, IGF-1, Myo-D, Myf-5, myogenin, and acetylcholine receptor (AChR) subunits α and β was found following treadmill training. Taken together, these results suggest that the upregulation of genes associated with neurite and AChR regeneration following treadmill training may contribute to enhanced gastrocnemius strength recovery following BoNT-A injection.http://dx.doi.org/10.1155/2013/593271 |
| spellingShingle | Sen-Wei Tsai Hsiao-Ling Chen Yi-Chun Chang Chuan-Mu Chen Molecular Mechanisms of Treadmill Therapy on Neuromuscular Atrophy Induced via Botulinum Toxin A Neural Plasticity |
| title | Molecular Mechanisms of Treadmill Therapy on Neuromuscular Atrophy Induced via Botulinum Toxin A |
| title_full | Molecular Mechanisms of Treadmill Therapy on Neuromuscular Atrophy Induced via Botulinum Toxin A |
| title_fullStr | Molecular Mechanisms of Treadmill Therapy on Neuromuscular Atrophy Induced via Botulinum Toxin A |
| title_full_unstemmed | Molecular Mechanisms of Treadmill Therapy on Neuromuscular Atrophy Induced via Botulinum Toxin A |
| title_short | Molecular Mechanisms of Treadmill Therapy on Neuromuscular Atrophy Induced via Botulinum Toxin A |
| title_sort | molecular mechanisms of treadmill therapy on neuromuscular atrophy induced via botulinum toxin a |
| url | http://dx.doi.org/10.1155/2013/593271 |
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