title: Apoptosis of oligodendrocytes occurs for long distances away from the primary injury after compression trauma to rat spinal cord.
abstract: We evaluated by in situ nick end labeling the presence of apoptotic glial cells in the spinal cord of rats which have sustained a moderate and severe compression injury at the level of T8-9, resulting in a severe but reversible paraparesis and irreversible paraplegia, respectively. In a previous investigation we found apoptotic glial cells (oligodendrocytes) in the immediate vicinity of the primary lesion (T7 and T10). The present study was designed to evaluate the extent of such cells in the spinal cord even at long distances away from the primary injury. Rats sustaining a moderate and severe compression injury and surviving 4 and 9 days showed a significant increase in the number of apoptotic glial cells at the T1, T5, T7, T12 and L2 levels. At the T10 level the elevation was significant only after day 9. There was no significant increase in the number of these cells at 4 h and 1 day after moderate and severe compression. In general, the apoptotic cells were most often seen in segments adjacent to the compression. They were randomly located in the ventral, lateral and dorsal tracts but were rarely present in the gray matter of the cord. In conclusion, compression trauma to rat spinal cord induces signs of apoptosis in glial cells, presumably oligodendrocytes of the long tracts. This newly discovered type of secondary injury is widely distributed in the damaged spinal cord and occurs even at long distances remote from the initial compression injury. Apoptotic cell death of oligodendrocytes will induce myelin degeneration and cause additional disturbances of axonal function. This cell damage may be a target for future therapy since it occurs after a delay and chemical compounds are now available by which apoptotic cell death can be modified.
authors.affiliation: Research Group in Neuropathology, Department of Genetics and Pathology, University Hospital, S-751 85 Uppsala, Sweden.
authors.forename: G L
authors.initials: GL
authors.lastname: Li
authors.forename: M
authors.initials: M
authors.lastname: Farooque
authors.forename: A
authors.initials: A
authors.lastname: Holtz
authors.forename: Y
authors.initials: Y
authors.lastname: Olsson
mesh_terms: D016564:Amyloid beta-Protein Precursor / Q000032:analysis; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D007211:Indoles; D008297:Male; D009836:Oligodendroglia / Q000473:pathology*; D051381:Rats; D013116:Spinal Cord / Q000473:pathology* / Q000503:physiopathology; D013117:Spinal Cord Compression / Q000473:pathology* / Q000503:physiopathology; D013997:Time Factors
chemical_list: D016564:Amyloid beta-Protein Precursor; D007211:Indoles; C018588:Luxol Fast Blue MBS