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Publication : Glycine receptor subunit-β-deficiency in a mouse model of spasticity results in attenuated physical performance, growth, and muscle strength.

First Author  Rivares C Year  2022
Journal  Am J Physiol Regul Integr Comp Physiol Volume  322
Issue  5 Pages  R368-R388
PubMed ID  35108108 Mgi Jnum  J:322493
Mgi Id  MGI:7257899 Doi  10.1152/ajpregu.00242.2020
Citation  Rivares C, et al. (2022) Glycine receptor subunit-ss -deficiency in a mouse model of spasticity results in attenuated physical performance, growth and muscle strength. Am J Physiol Regul Integr Comp Physiol
abstractText  Spasticity is the most common neurological disorder associated with increased muscle contraction causing impaired movement and gait. The aim of this study was to characterize the physical performance, skeletal muscle function and phenotype of mice with a hereditary spastic mutation (B6.Cg-Glrb(spa)/J). Motor function, gait and physical activity of juvenile and adult spastic mice and the morphological, histological and mechanical characteristics of their soleus and gastrocnemius medialis muscles were compared with their wild-type (WT) littermates. Spastic mice showed attenuated growth, impaired motor function and low physical activity. Gait of spastic mice was characterized by a typical hopping pattern. Spastic mice showed lower muscle forces, which were related to the smaller physiological cross-sectional area of spastic muscles. The muscle-tendon complex length-force relationship of adult gastrocnemius medialis was shifted towards shorter lengths, which was explained by attenuated longitudinal tibia growth. Spastic gastrocnemius medialis was more fatigue resistant than WT gastrocnemius medialis. This was largely explained by a higher mitochondrial content in muscle fibers and relatively higher percentage of slow-type muscle fibers. Muscles of juvenile spastic mice showed similar differences compared with WT juvenile mice, but these were less pronounced than between adult mice. This study shows that in spastic mice, disturbed motor function and gait is likely to be the result of hyperactivity of skeletal muscle and impaired skeletal muscle growth, which progress with age.
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