Proliferation of mature oligodendrocytes after trauma to the central nervous system

Abstract

It has long been thought that mature oligodendrocytes in the adult mammalian central nervous system (CNS) are post-mitotic and are unable to proliferate in response to injury. The implications of this have been profound, because it has been suggested that this failure of oligodendrocytes to undergo mitosis is perhaps one of the reasons for the failure of the human CNS to undergo remyelination after demyelinating disease. This is in contrast with the normal peripheral nervous system in which there is consistent remyelination, and brisk Schwann cell mitosis. Although it has recently been shown that oligodendrocytes can be regenerated following some specific instances of demyelination^1–3, it has long been accepted that unlike mature astrocytes and microglia (macrophages), oligodendrocytes do not proliferate in response to general conditions damaging nervous system^4,5. Here we show that mature oligodendrocytes in adult animals, as well as astrocytes and microglia, are able to respond to damage in the CNS following trauma by incorporating tritiated thymidine into their nuclei.