• M Farooque, J Isaksson, and Y Olsson.
• Research Group of Neuropathology, Department of Genetics and Pathology, Uppsala University Hospital, Sweden.
• Acta Neuropathol. 2001 Aug 1; 102 (2): 132-40.

AbstractWe have previously demonstrated that mice deficient in ICAM-1 and P-selectin (ICAM-1/PS-/-) have improved functional recovery after spinal cord injury (SCI), compared to injured controls. In this study the spinal cords from wild-type and ICAM-1/PS-/- mice were evaluated histopathologically 14 days after severe compression-type SCI. Following injury there was an atrophy of the spinal cord. Significant sparing of total cross-sectional area was noted in ICAM-1/PS-/- mice compared to injured controls at the site of compression and in the distal peri-injury zone. Likewise, significant preservation of white matter area, as measured by Luxol staining, was found in mutant mice at the site of injury and in the proximal peri-injury zone. Gray matter damage was investigated by microtubule-associated protein 2 immunohistochemistry. Following severe SCI, a trend of gray matter sparing was noticed in ICAM-1/PS-/- animals. Quantitation of iba1 immunohistochemistry revealed that microglial reaction was significantly suppressed in the mutant animals. Astroglial reaction, visualized by GFAP immunostaining, did not differ between groups. Our results indicate that ICAM-1 and P-selectin are involved in autodestructive events provoked by the initial injury but the precise underlying mechanisms remain obscure.

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