Neuroscience 2004 Abstract
Presentation Number: | 494.17 |
---|---|
Abstract Title: | Altered oligodendrocyte behavior following contact with axonal plasma membrane. |
Authors: |
Becker-Catania, S. G.*1,2
; Nelson, J. K.1,2
; De Vries, G. H.1,2
1Edward Hines Jr. VA Hosp., Hines, IL 2IL, 5th Avenue and Roosevelt Rd., 60141, |
Primary Theme and Topics |
Development - Neurogenesis and Gliogenesis -- Neuron-glia interactions |
Session: |
494. Neuron--Glia Interactions in Development: Schwann Cells and Oligodendrocytes Poster |
Presentation Time: | Monday, October 25, 2004 1:00 PM-2:00 PM |
Location: | San Diego Convention Center - Hall A-H, Board # D2 |
Keywords: | DIFFERENTIATION, PROLIFERATION, MAP KINASE, IMMUNOCYTOCHEMISTRY |
In multiple sclerosis (MS), oligodendrocyte progenitor cells (OPCs) fail to properly differentiate and remyelinate axons. It is thought that axonal-derived molecular signals control OPC migration, proliferation, differentiation, and ultimately myelination. Using an in vitro model of axon-glial interaction, we looked for changes in OPC proliferation and differentiation following treatment with a membrane preparation enriched in axonal plasma membrane (AEF). A dose-dependent increase in OPC proliferation was observed following exposure to AEF that persisted up to 72 hours post-AEF treatment. Elevated MAP kinase levels were detected as early as 5 minutes and were sustained throughout the 72 hour endpoint. Interestingly, a specific tropism and binding of the AEF to the OPC cell bodies and processes was observed within 24 hours. AEF-treated OPCs retained a more immature morphology as evidenced by fewer, less-extensively branched, and finer processes. Immunocytochemistry using a spectrum of developmentally-expressed oligodendrocyte-selective markers, showed that untreated OPCs differentiated and expressed high levels of CNPase, GalC, O4 and MBP that colocalized on the cell body and processes. Expression of immature oligodendrocyte (OLG) markers such as nestin and A2B5 were reduced. In contrast, AEF-treated OPCs had greater expression of immature cell markers such as nestin and A2B5 and fewer cells that expressed more mature OLG markers at 24, 48 and 72 hours. AEF or microsomal fractions prepared from MS plaque and adjacent areas induced an increase in OPC MAP kinase within 15 minutes. These observations support a mechanism by which axonal growth factors signal through MAP kinase and sustain proliferation, thereby preventing OPC differentiation and subsequent myelination.
Supported by NIH grant NS043419-02
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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