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A study of juvenile rat spinal cord injury
Author(s) -
Wingrave J. M.,
Matzelle D. D.,
Wilford G. G.,
Hogan E. L.,
Banik N. L.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.81.s1.41_4.x
Subject(s) - juvenile , spinal cord , spinal cord injury , medicine , western blot , young adult , cord , calpain , anesthesia , chemistry , biology , surgery , psychiatry , biochemistry , genetics , gene , enzyme
Greater than 5% of all spinal cord injuries (SCI) in the US occur in people younger than 16, although a minority, children will require extended attention during their lifetime. While facing increased mortality in the initial 24 h after trauma, children with incomplete injuries seem to have a greater capacity for recovery of function compared to adults suggesting that there is a difference in injury tolerance in the young over the adult. Knowledge of the factors involved in this difference would not only increase understanding of SCI, but also potentiate new avenues for SCI treatment. Yet there has not been a model for the study of youth SCI. For these reasons, we developed a model of SCI in juvenile rats equivalent to an adult injury of 25 g cm force (GCF). To do so, we recorded spinal cord masses of Sprague–Dawley rats at 21, 30, 45, and 60 days of age, compared them to adult cord masses, and assembled a conversion factor that provides youth injuries comparable to adult. To investigate the pathophysiology in juvenile SCI, two cord segments, 1 cm long, were removed from animals 24 h following injury. One segment was centered at the impact site, the other immediately caudal. After homogenization, the samples were assayed by Western blot analysis for calpain content and degradation of 68K Neuro‐Filament Protein (68K NFP), a neuronal structural protein. mCalpain expression, a neutral protease previously implicated in secondary SCI, was reduced in juvenile animals relative to adult cohorts. The degradation of 68K NFP was also found to be reduced in juvenile animals. From these analyses, it seems plausible that calpain expression and pathogenic activity is abated in the setting of young rat SCI. Acknowledgements: Supported by grants from NIH‐NINDS.