Literature DB >> 17122320

Spastic tail muscles recover from myofiber atrophy and myosin heavy chain transformations in chronic spinal rats.

R Luke W Harris1, Charles T Putman, Michelle Rank, Leo Sanelli, David J Bennett.   

Abstract

Without intervention after spinal cord injury (SCI), paralyzed skeletal muscles undergo myofiber atrophy and slow-to-fast myofiber type transformations. We hypothesized that chronic spasticity-associated neuromuscular activity after SCI would promote recovery from such deleterious changes. We examined segmental tail muscles of chronic spinal rats with long-standing tail spasticity (7 mo after sacral spinal cord transection; older chronic spinals), chronic spinal rats that experienced less spasticity early after injury (young chronic spinals), and rats without spasticity after transection and bilateral deafferentation (spinal isolated). These were compared with tail muscles of age-matched normal rats. Using immunohistochemistry, we observed myofiber distributions of 15.9 +/- 3.5% type I, 18.7 +/- 10.7% type IIA, 60.8 +/- 12.6% type IID(X), and 2.3 +/- 1.3% type IIB (means +/- SD) in young normals, which were not different in older normals. Young chronic spinals demonstrated transformations toward faster myofiber types with decreased type I and increased type IID(X) paralleled by atrophy of all myofiber types compared with young normals. Spinal isolated rats also demonstrated decreased type I myofiber proportions and increased type II myofiber proportions, and severe myofiber atrophy. After 4 mo of complete spasticity (older chronic spinals), myofiber type transformations were reversed, with no significant differences in type I, IIA, IID(X), or IIB proportions compared with age-matched normals. Moreover, after this prolonged spasticity, type I, IIA, and IIB myofibers recovered from atrophy, and type IID(X) myofibers partially recovered. Our results indicate that early after transection or after long-term spinal isolation, relatively inactive tail myofibers atrophy and transform toward faster myofiber types. However, long-term spasticity apparently produces neuromuscular activity that promotes recovery of myofiber types and myofiber sizes.

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Year:  2006        PMID: 17122320      PMCID: PMC5759973          DOI: 10.1152/jn.00622.2006

Source DB:  PubMed          Journal:  J Neurophysiol        ISSN: 0022-3077            Impact factor:   2.714


  50 in total

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2.  Persistence of hybrid fibers in rat soleus after spinal cord transection.

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4.  Long-term effects of spinal cord transection on fast and slow rat skeletal muscle. I. Contractile properties.

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Review 5.  Alterations in synaptic input to motoneurons during partial spinal cord injury.

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6.  Lumbosacral spinal isolation in cat: surgical preparation and health maintenance.

Authors:  L Eldridge
Journal:  Exp Neurol       Date:  1984-02       Impact factor: 5.330

7.  Satellite cell proliferation in low frequency-stimulated fast muscle of hypothyroid rat.

Authors:  C T Putman; S Düsterhöft; D Pette
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8.  Soleus motor units in chronic spinal transected cats: physiological and morphological alterations.

Authors:  T C Cope; S C Bodine; M Fournier; V R Edgerton
Journal:  J Neurophysiol       Date:  1986-06       Impact factor: 2.714

9.  Early changes in muscle fiber size and gene expression in response to spinal cord transection and exercise.

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10.  Effects of spaceflight on myosin heavy-chain content, fibre morphology and succinate dehydrogenase activity in rat diaphragm.

Authors:  Gregory Hansen; Karen J B Martinuk; Gordon J Bell; Ian M MacLean; Thomas P Martin; Charles T Putman
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  9 in total

1.  Changes in motoneuron properties following spinal cord transection: does afferent input play a role?

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2.  Demystifying Spasticity: Reply to Dietz.

Authors:  D J Bennett
Journal:  J Neurophysiol       Date:  2008-02       Impact factor: 2.714

3.  Spasticity and preservation of skeletal muscle mass in people with spinal cord injury.

Authors:  Seungwoo Cha; Jae-Hyun Yun; Youho Myong; Hyung-Ik Shin
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4.  Relationship of spasticity to soft tissue body composition and the metabolic profile in persons with chronic motor complete spinal cord injury.

Authors:  Ashraf S Gorgey; Anthony E Chiodo; Eric D Zemper; Joseph E Hornyak; Gianna M Rodriguez; David R Gater
Journal:  J Spinal Cord Med       Date:  2010       Impact factor: 1.985

5.  Supraspinal and Afferent Signaling Facilitate Spinal Sensorimotor Network Excitability After Discomplete Spinal Cord Injury: A Case Report.

Authors:  Alena Militskova; Elvira Mukhametova; Elsa Fatykhova; Safar Sharifullin; Carlos A Cuellar; Jonathan S Calvert; Peter J Grahn; Tatiana Baltina; Igor Lavrov
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6.  Does elimination of afferent input modify the changes in rat motoneurone properties that occur following chronic spinal cord transection?

Authors:  Duane C Button; Jayne M Kalmar; Kalan Gardiner; Tanguy Marqueste; Hui Zhong; Roland R Roy; V Reggie Edgerton; Phillip F Gardiner
Journal:  J Physiol       Date:  2007-11-15       Impact factor: 5.182

7.  Severe spasticity in lower extremities is associated with reduced adiposity and lower fasting plasma glucose level in persons with spinal cord injury.

Authors:  I-Y Jung; H-R Kim; S M Chun; J-H Leigh; H-I Shin
Journal:  Spinal Cord       Date:  2016-09-13       Impact factor: 2.772

Review 8.  Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity.

Authors:  Jessica M D'Amico; Elizabeth G Condliffe; Karen J B Martins; David J Bennett; Monica A Gorassini
Journal:  Front Integr Neurosci       Date:  2014-05-12

9.  Motor unit firing rates during spasms in thenar muscles of spinal cord injured subjects.

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  9 in total

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