Axonal degeneration stimulates the formation of NG2+ cells and oligodendrocytes in the mouse.

Published

Journal Article

Proliferation of the adult NG2-expressing oligodendrocyte precursor cells has traditionally been viewed as a remyelination response ensuing from destruction of myelin and oligodendrocytes, and not to the axonal pathology that is also a characteristic of demyelinating disease. To better understand the response of the NG2+ cells to the different components of demyelinating pathology, we investigated the response of adult NG2+ cells to axonal degeneration in the absence of primary myelin or oligodendrocyte pathology. Axonal degeneration was induced in the hippocampal dentate gyrus of adult mice by transection of the entorhino-dentate perforant path projection. The acutely induced degeneration of axons and terminals resulted in a prompt response of NG2+ cells, consisting of morphological transformation, cellular proliferation, and upregulation of NG2 expression days 2-3 after surgery. This was followed by a reduction of cellular NG2 expression to subnormal levels from day 5 to 7 and reappearance of normal appearing NG2+ cells from day 10. Mice that had received repeated injections of bromodeoxyuridine from 24 to 72 h after surgery contained significant numbers of bromodeoxyuridine-incorporating oligodendrocytes in the areas with axonal degeneration at day 7. The results suggest that axonal degeneration induces a unique sequence of changes of NG2+ cells and that a subpopulation of the newly generated NG2+ cells differentiate into oligodendrocytes.

Full Text

Cited Authors

  • Nielsen, HH; Ladeby, R; Drøjdahl, N; Peterson, AC; Finsen, B

Published Date

  • August 2006

Published In

Volume / Issue

  • 54 / 2

Start / End Page

  • 105 - 115

PubMed ID

  • 16718683

Pubmed Central ID

  • 16718683

Electronic International Standard Serial Number (EISSN)

  • 1098-1136

International Standard Serial Number (ISSN)

  • 0894-1491

Digital Object Identifier (DOI)

  • 10.1002/glia.20357

Language

  • eng