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.

journal_name

Acta Neuropathol

journal_title

Acta neuropathologica

authors

Li GL,Farooque M,Holtz A,Olsson Y

doi

10.1007/s004010051112

subject

Has Abstract

pub_date

1999-11-01 00:00:00

pages

473-80

issue

5

eissn

0001-6322

issn

1432-0533

pii

90980473.401

journal_volume

98

pub_type

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