A simple protocol for assessing inter-trial and inter-examiner reliability for two noninvasive measures of limb muscle strength

Carlson, C. George; Rutter, John; Bledsoe, Cathy; Singh, Rajvir; Hoff, Helena; Bruemmer, Kay; Sesti, Jenna; Gatti, Francesca; Berge, Jonas; McCarthy, Laura

doi:10.1016/j.jneumeth.2009.11.006

Cited by 42 publications

(45 citation statements)

References 12 publications

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“…2E,F; p Ͻ 0.01). Supporting this model, hyperactivating and loss-of-function mutations in ␣2-chimaerin that respectively decrease or increase Rac1 signaling cause axon guidance defects in humans and in mouse and zebrafish models (Beg et al, 2007;Iwasato et al, 2007;Wegmeyer et al, 2007;Miyake et al, 2008;Clark et al, 2013). These results demonstrate that ␣2-chimaerin is essential for lateral LMC axon repulsion from ephrin-A, but not for medial LMC repulsion from ephrin-B.…”

Section: ␣2-chimaerin Is Required For Ephrin-a-mediated Motor Axon Rementioning

confidence: 97%

“…Last, to assess limb muscle strength and coordination, we used an inverted screen test requiring animals to hang and support their body weight by grasping a wire grid for an extended period of time (Carlson et al, 2010). In this assay, ␣2 gt/gt mutants grasped the screen for the same amount of time as control littermates ( Fig.…”

Section: Lmc Axonal Miswiring Persists In Adult ␣2-chimaerin Mutantsmentioning

confidence: 99%

“…Structural diversity of GAPs and GEFs enables them to interact preferentially with selected axon guidance receptors, whereas their conserved domains enable coupling to a limited set of Rho GTPases. For example, ephexin1 and Vav2 are GEFs specific for EphA and EphB receptors required for RhoA and Rac1 activation, respectively (Shamah et al, 2001;Cowan et al, 2005). ␣2-chimaerin is a Rac1-inactivating GAP, binding Ephs from both A and B classes (Beg et al, 2007;Iwasato et al, 2007;Shi et al, 2007;Wegmeyer et al, 2007), suggesting that it might be a universal effector of Eph signaling.…”

Section: Introductionmentioning

confidence: 99%

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α2-Chimaerin Is Required for Eph Receptor-Class-Specific Spinal Motor Axon Guidance and Coordinate Activation of Antagonistic Muscles

et al. 2015

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Axonal guidance involves extrinsic molecular cues that bind growth cone receptors and signal to the cytoskeleton through divergent pathways. Some signaling intermediates are deployed downstream of molecularly distinct axon guidance receptor families, but the scope of this overlap is unclear, as is the impact of embryonic axon guidance fidelity on adult nervous system function. Here, we demonstrate that the Rho-GTPase-activating protein ␣2-chimaerin is specifically required for EphA and not EphB receptor signaling in mouse and chick spinal motor axons. Reflecting this specificity, the loss of ␣2-chimaerin function disrupts the limb trajectory of extensor-muscleinnervating motor axons the guidance of which depends on EphA signaling. These embryonic defects affect coordinated contraction of antagonistic flexor-extensor muscles in the adult, indicating that accurate embryonic motor axon guidance is critical for optimal neuromuscular function. Together, our observations provide the first functional evidence of an Eph receptor-class-specific intracellular signaling protein that is required for appropriate neuromuscular connectivity.

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Section: ␣2-chimaerin Is Required For Ephrin-a-mediated Motor Axon Rementioning

confidence: 97%

Section: Lmc Axonal Miswiring Persists In Adult ␣2-chimaerin Mutantsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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α2-Chimaerin Is Required for Eph Receptor-Class-Specific Spinal Motor Axon Guidance and Coordinate Activation of Antagonistic Muscles

et al. 2015

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“…These physiological characteristics are similar to those of aged mice and indicate that some characteristics of sarcopenia are present in this progeroid mouse model. In mice that are aged normally and in the Zmpste24 −/− mouse model of accelerated aging, force generation as well as rates of muscle contraction are impaired (Brooks and Faulkner 1988;Moran et al 2005), as are parameters of neuromuscular performance (Carlson et al 2010;Ingram 2000). Collectively, these results suggest that skeletal muscle is an affected tissue in HGPS.…”

Section: Discussionmentioning

confidence: 89%

Skeletal muscle contractile function and neuromuscular performance in Zmpste24 −/− mice, a murine model of human progeria

Greising

Call

Lund

et al. 2011

AGE

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Human progeroid syndromes and premature aging mouse models present as segmental, accelerated aging because some tissues and not others are affected. Skeletal muscle is detrimentally changed by normal aging but whether it is an affected tissue in progeria has not been resolved. We hypothesized that mice which mimic Hutchinson-Gilford progeria syndrome would exhibit age-related alterations of skeletal muscle. Zmpste24 −/− and Zmpste24 +/+ littermates were assessed for skeletal muscle functions, histo-morphological characteristics, and ankle joint mechanics. Twenty-four-hour active time, ambulation, grip strength, and whole body tension were evaluated as markers of neuromuscular performance, each of which was at least 33% lower in Zmpste24 −/− mice compared with littermates (p<0.06). Contractile capacity of the posterior leg muscles were not affected in Zmpste24 −/− mice, but muscles of the anterior leg were 30-90% weaker than those of Zmpste24 +/+ mice (p< 0.01). Leg muscles were 32-47% smaller in the Zmpste24 −/− mice and contained~60% greater collagen relative to littermates (p<0.01). Soleus and extensor digitorum longus muscles of Zmpste24 −/− mice had excessive myonuclei and altered fiber size distributions but, otherwise, appeared normal. Ankle range of motion was 70% lower and plantar-and dorsiflexion passive torques were nearly 3-fold greater in Zmpste24 −/− than Zmpste24 +/+ mice (p≤0.01). The combined factors of muscle atrophy, collagen accumulation, and perturbed joint mechanics likely contributed to poor neuromuscular performance and selective muscle weakness displayed by Zmpste24 −/− mice. In summary, these characteristics are similar to those of aged mice indicating accelerated aging of skeletal muscle in progeria.Keywords Aging . Lamin . Range of motion . Sarcopenia . Strength Abbreviations EDLExtensor digitorum longus HGPS Hutchinson-Gilford progeria syndrome P o Maximal isometric tetanic force ROM Range of motion AGE (2012) 34:805-819

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“…In particular, this test has been widely utilized to determine the natural course of neuromuscular disease, to demonstrate neuromuscular impairment and the lack of coordination or to study the effects of genetic or pharmacologic treatments on skeletal muscle functionality. 22 Four limb hang testing would also be amenable to studies of age-related neuromuscular decline.…”

Section: Four Limb-hanging Testmentioning

confidence: 99%

Assessment of muscle mass and strength in mice

2015

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Muscle weakness is an important phenotype of many diseases that is linked to impaired locomotion and increased mortality. The force that a muscle can generate is determined predominantly by muscle size, fiber type and the excitation-contraction coupling process. Here we describe methods for the histological assessment of whole muscle to determine fiber cross-sectional area and fiber type, determination of changes in myocyte size using C2C12 cells, in vivo functional tests and measurement of contractility in dissected whole muscles. The extensor digitorum longus and soleus muscles are ideally suited for whole-muscle contractility, and dissection of these muscles is described.

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A simple protocol for assessing inter-trial and inter-examiner reliability for two noninvasive measures of limb muscle strength

Cited by 42 publications

References 12 publications

α2-Chimaerin Is Required for Eph Receptor-Class-Specific Spinal Motor Axon Guidance and Coordinate Activation of Antagonistic Muscles

α2-Chimaerin Is Required for Eph Receptor-Class-Specific Spinal Motor Axon Guidance and Coordinate Activation of Antagonistic Muscles

Skeletal muscle contractile function and neuromuscular performance in Zmpste24 −/− mice, a murine model of human progeria

Assessment of muscle mass and strength in mice

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