Astrocytes and oligodendrocytes reactions after a total section of the rat spinal cord.

Regeneration after an injury in the Central Nervous System is dependent on intrinsic and extrinsic factors. Among the latter are the reactions of glial cells. Using the model of total section of adult rat spinal cord, we have studied the spatial and temporal responses of astrocytes and oligodendrocytes to the lesion of spinal cord axons. We studied at molecular and cellular levels the specific markers GFAP (glial fibrillary acidic protein) for the astrocytes, CNP (2'-3' cyclic 3' nucleotide phosphodiesterase) which is principally expressed by immature oligodendrocytes, and MBP (myelin basic protein) implicated later in the myelin compaction, and which is more specific of mature oligodendrocytes. After injury, all astrocytes, but more markedly those of the grey matter, reacted by an increase of GFAP messenger and protein. This increase was very rapid for messenger, and peaked at 3 days. This increase was more protracted for the protein and persisted after 3 weeks. Messenger increase is more marked and more protracted below than above the lesion. Oligodendrocytes also reacted quickly by an increase of CNP and MBP messengers. For CNP, both messenger and protein increased rapidly and returned to control level after 1 week. MBP showed the same time course of changes, with lower and slower decrease above the lesion. Counts of oligodendrocytes showed that the percentage of the less mature form (light oligodendrocytes) increased dramatically above and below the lesion. After 1 week, above the lesion, this percentage was well below that of the control, whereas below the lesion, it reverted to control value. These results indicate that, following a lesion, astrocytes react quickly and intensely, but more so below the lesion; oligodendrocytes resume a sequence of maturation which is eventually completed above the lesion where remyelinisation can occur and which is prematurely interrupted below the lesion. However, intact oligodendrocytes persist below the lesion, where they constitute a potential for remyelinisation of regenerated and/or transplanted axons.