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Response of the oligodendrocyte progenitor cell population (defined by NG2 labelling) to demyelination of the adult spinal cord

✍ Scribed by Hans S. Keirstead; Joel M. Levine; William F. Blakemore


Publisher
John Wiley and Sons
Year
1998
Tongue
English
Weight
342 KB
Volume
22
Category
Article
ISSN
0894-1491

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✦ Synopsis


Elucidation of the response of oligodendrocyte progenitor cell populations to demyelination in the adult central nervous system (CNS) is critical to understanding why remyelination fails in multiple sclerosis. Using the anti-NG2 monoclonal antibody to identify oligodendrocyte progenitor cells, we have documented their response to antibody-induced demyelination in the dorsal column of the adult rat spinal cord. The number of NG2ϩ cells in the vicinity of demyelinated lesions increased by 72% over the course of 3 days following the onset of demyelination. This increase in NG2ϩ cell numbers did not reflect a nonspecific staining of reactive cells, as GFAP, OX-42, and Rip antibodies did not co-localise with NG2ϩ cells in double immunostained tissue sections. NG2ϩ cells incorporated BrdU 48-72 h following the onset of demyelination. After the onset of remyelination (10-14 days), the number of NG2ϩ cells decreased to 46% of control levels and remained consistently low for 2 months. When spinal cords were exposed to 40 Grays of x-irradiation prior to demyelination, the number of NG2ϩ cells decreased to 48% of control levels by 3 days following the onset of demyelination and remained unchanged at 3 weeks. Since 40 Grays of x-irradiation kills dividing cells, these studies illustrate a responsive and nonresponsive NG2ϩ cell population following demyelination in the adult spinal cord and suggest that the responsive NG2ϩ cell population does not renew itself.


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✍ David P. Crockett; Mark Burshteyn; Corina Garcia; Michela Muggironi; Patrizia Ca 📂 Article 📅 2004 🏛 John Wiley and Sons 🌐 English ⚖ 720 KB

## Abstract Remyelination is a critical step for recovery of function after demyelination and defines the ability to generate new myelin. This repair process is dependent on the presence of resident oligodendrocyte progenitors (OLPs) that have been shown to remyelinate axons after demyelination. We