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Skeletal muscle deficits following spinal cord injury in a new rat model
Author(s) -
Ye Fan,
Baligand Celine,
Vohra Ravneet,
Keener Jonathon,
Bose Prodip,
Walter Glenn,
Thompson Floyd,
Vandenborne Krista
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1105.15
Subject(s) - hindlimb , spinal cord injury , medicine , muscle atrophy , anatomy , atrophy , spinal cord , rat model , amyotrophy , extensor digitorum longus muscle , paraplegia , physical medicine and rehabilitation , skeletal muscle , anesthesia , psychiatry
Spontaneous recovery in contusion spinal cord injury (SCI) animal models is a limitation in preclinical rehabilitation studies. The objective of this study was to test a new cast immobilization (IMM) rat model of SCI, in which IMM minimizes muscle activation and loading of hindlimbs. Sprague Dawley female rats (16‐week old) were randomly assigned into three groups: 1) controls, 2) SCI and 3) SCI plus cast immobilization (SCI+IMM). Severe contusions were performed at the T8 level by a NYU impactor (10g, 50mm weight drop). For SCI+IMM, joints of the lower body were immobilized at resting angles with casting tape after 1 week of SCI. Following 3 weeks of intervention, muscle mass and contractile properties were assessed. Muscle mass was reduced by 34% in soleus, 22% in gastrocnemius, 16% tibialis anterior and 13% in extensor digitorum longus in SCI. IMM induced an additional atrophy of 15% to 20% in both anterior and posterior compartments of hindlimb muscles. Maximal tetanic force was reduced by 30% in SCI and 50% in SCI+IMM. However, specific force was not different. Muscles in SCI+IMM showed shorter time to peak tension and half‐relaxation time compared to SCI and controls. These preliminary results indicate that unloading of the muscles after SCI+IMM leads to profound muscle atrophy and loss of force capabilities of the hindlimb muscles without spontaneous recovery. NICHD PO1 HD059751 ‐01A1 supports this work.