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. 2019 Nov 13;9:16699. doi: 10.1038/s41598-019-53235-w

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Longitudinal forelimb (A–C) and hindlimb (D–F) electrophysiology assessment demonstrated rapid loss of motor unit connectivity in mutant SOD1 rats. Additionally, longitudinal plantar flexion muscle contractility assessment (G–J) demonstrated rapid loss of torque in mutant SOD1 rats, which was closely correlated with hindlimb electrophysiological measures (K–N). There were rapid changes in (A) forelimb compound muscle action potential amplitude (p = 0.157), and (C) forelimb motor unit number estimation was significantly reduced (p = 0.008), but (B) forelimb single motor unit potential amplitude (p = 0.541) was not significantly changed. By contrast, (D) hindlimb compound muscle action potential amplitude (p < 0.0001), (E) hindlimb single motor unit potential amplitude (p = 0.015), and (F) hindlimb motor unit number estimation (p < 0.001) all exhibited significant decline over 20 days after baseline. Mutant SOD1 females (n = 3) are presented as and mutant SOD1 males (n = 5) as . For electrophysiology data, repeated measure one-way ANOVA with Dunnett’s multiple comparison tests was used to compare assessments at 10 days and 20 days to baseline. Adjusted p values for Dunnett’s multiple comparison tests are illustrated: *p < 0.05, **p < 0.01, ***p < 0.001. Following baseline hindlimb contractility measurements there was rapid loss of (G) twitch (p = 0.0004) and (H) tetanic (p = 0.0009) contractility. Similarly, when normalised to body mass, (I) normalised twitch, (p < 0.0001) and (J) normalised tetanic (p < 0.0001) contractility were reduced. Females (n = 3) are shown as and males (n = 5) as . For muscle contractility data, repeated measure one-way ANOVA with Dunnett’s multiple comparison tests was used to compare assessments at 10 days and 20 days to baseline. Adjusted p values for Dunnett’s multiple comparison tests are illustrated: *<0.05, **<0.01, ***<0.001. Plantarflexion muscle contractility was tightly associated with (K,L) compound muscle action potential (CMAP) amplitude (twitch: r = 0.868, p < 0.0001; tetanic: r = 0.911, p < 0.0001) and (M,N) motor unit number, as determined by Motor Unit Number Estimation (MUNE), (twitch: r = 0.633, p = 0.0005; tetanic: r = 0.845 p < 0.0001) in mutant male and female SOD1 rats.

Inline graphic — Longitudinal forelimb (A–C) and hindlimb (D–F) electrophysiology assessment demonstrated rapid loss of motor unit connectivity in mutant SOD1 rats. Additionally, longitudinal plantar flexion muscle contractility assessment (G–J) demonstrated rapid loss of torque in mutant SOD1 rats, which was closely correlated with hindlimb electrophysiological measures (K–N). There were rapid changes in (A) forelimb compound muscle action potential amplitude (p = 0.157), and (C) forelimb motor unit number estimation was significantly reduced (p = 0.008), but (B) forelimb single motor unit potential amplitude (p = 0.541) was not significantly changed. By contrast, (D) hindlimb compound muscle action potential amplitude (p < 0.0001), (E) hindlimb single motor unit potential amplitude (p = 0.015), and (F) hindlimb motor unit number estimation (p < 0.001) all exhibited significant decline over 20 days after baseline. Mutant SOD1 females (n = 3) are presented as and mutant SOD1 males (n = 5) as . For electrophysiology data, repeated measure one-way ANOVA with Dunnett’s multiple comparison tests was used to compare assessments at 10 days and 20 days to baseline. Adjusted p values for Dunnett’s multiple comparison tests are illustrated: *p < 0.05, **p < 0.01, ***p < 0.001. Following baseline hindlimb contractility measurements there was rapid loss of (G) twitch (p = 0.0004) and (H) tetanic (p = 0.0009) contractility. Similarly, when normalised to body mass, (I) normalised twitch, (p < 0.0001) and (J) normalised tetanic (p < 0.0001) contractility were reduced. Females (n = 3) are shown as and males (n = 5) as . For muscle contractility data, repeated measure one-way ANOVA with Dunnett’s multiple comparison tests was used to compare assessments at 10 days and 20 days to baseline. Adjusted p values for Dunnett’s multiple comparison tests are illustrated: *<0.05, **<0.01, ***<0.001. Plantarflexion muscle contractility was tightly associated with (K,L) compound muscle action potential (CMAP) amplitude (twitch: r = 0.868, p < 0.0001; tetanic: r = 0.911, p < 0.0001) and (M,N) motor unit number, as determined by Motor Unit Number Estimation (MUNE), (twitch: r = 0.633, p = 0.0005; tetanic: r = 0.845 p < 0.0001) in mutant male and female SOD1 rats.