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Increased fatigue resistance and preserved specific force in intact single muscle fibres from the SOD1G93A mouse model of ALS
Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet, Stockholm, Sweden.ORCID-id: 0000-0002-5322-4150
Karolinska Institutet, Stockholm, Sweden.
Vise andre og tillknytning
2017 (engelsk)Inngår i: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 219, nr S710, s. 17-17, artikkel-id P-28Artikkel i tidsskrift, Meeting abstract (Fagfellevurdert) Published
Abstract [en]

Introduction: Amyotrophic lateral sclerosis (ALS) is a motor neurone disease characterized by degeneration and loss of motor neurones, leading to severe muscle weakness and paralysis. Although motor neurone degeneration is already a well-characterized symptom that contributes to muscle weakness in the SOD1G93A mouse model of ALS, the purpose of the current study was to determine whether muscle weakness in ALS can be attributed to impaired intrinsic force generation in skeletal muscles of SOD1G93A mice.

Methods: Experiments were performed on whole muscles and mechanically dissected intact single fibres from the flexor digitorum brevis (FDB) muscle of SOD1G93A mice at three age groups of 50, 125 and 150 days of age (P50, P125 and P150). Myoplasmic free [Ca2+] ([Ca2+]i) was measured using the fluorescent indicator, indo-1.

Results: Motor neurone loss and decreased force were evident in whole FDB muscles of P125–150 mice. In the intact single muscle fibres however, specific force, tetanic [Ca2+]iand resting [Ca2+]i were similar in single FDB fibres from symptomatic P125–150 SOD1G93A and age-matched wild-type littermates. The most intriguing finding was a markedly greater fatigue resistance in single fibres from P125–150 SOD1G93A vs. wild-type mice, which was not present in asymptomatic young P50 SOD1G93A mice. No shift in fibre-type distribution was observed in whole FDB muscles to explain the increased fatigue resistance of single fibres from P125–150 SOD1G93A mice.

Conclusion: These results support the hypothesis that muscle weakness in ALS is not attributed to intrinsicdefects in skeletal muscle fibre force generation.

sted, utgiver, år, opplag, sider
Wiley-Blackwell, 2017. Vol. 219, nr S710, s. 17-17, artikkel-id P-28
HSV kategori
Identifikatorer
URN: urn:nbn:se:oru:diva-66327ISI: 000393916600033OAI: oai:DiVA.org:oru-66327DiVA, id: diva2:1194893
Konferanse
Annual Meeting of the Scandinavian Physiological Society, Oslo, Norway, August 26-28, 2016
Tilgjengelig fra: 2018-04-04 Laget: 2018-04-04 Sist oppdatert: 2018-04-06bibliografisk kontrollert

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