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Neuroinflammation in a Forceps Compression Model of Spinal Cord Injury
Author(s) -
Vaughn Chloe N.,
Henley Jessica B.,
Iafrate Julia,
Stevenson Edward,
Jones T. Bucky
Publication year - 2010
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.24.1_supplement.640.4
Subject(s) - spinal cord injury , medicine , spinal cord , cord , neuroinflammation , spinal cord compression , traumatic injury , forceps , anesthesia , inflammation , surgery , psychiatry
We sought to evaluate the neuroinflammatory response in a compression model of spinal cord injury (SCI). Because compression is a common mechanism of injury in human spinal cord trauma, such a model has clinical relevance. In this study we used forceps to induce lateral compression injury to the spinal cord, producing a moderate degree of injury as previously described in the contusion model (Basso et al., 1996). Post‐injury inflammation has been implicated in secondary degeneration but has not been characterized in this model. We evaluated the inflammatory response in the injured spinal cord using immunohistochemistry. We found that neutrophils are present within the lesion site by 1 day post injury (dpi) but do not persist past 3 dpi. T‐cells were present by 1 dpi, mainly in gray matter at the epicenter. They peaked in number at 7 dpi, but persisted to 42 dpi. A similar time course was observed for macrophage activation, although the response was more widespread at the impact site and extended further rostrocaudally. Overall, we confirm that forceps compression of the spinal cord produces a neuroinflammatory response similar to what has been described in human spinal cord trauma and in contusion models of experimental spinal cord trauma. Thus, forceps compression represents a clinically relevant experimental model for evaluating secondary injury. Grant Funding Source : MWU Biomedical Sciences program