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Pathophysiology of oligodendroglial excitotoxicity
A Yoshioka1, B Bacskai, D Pleasure
1Division of Neurology, Children's Hospital of Philadelphia, PA 19104, USA.
Journal of Neuroscience Research
|November 15, 1996
Summary
Oligodendrocyte-like cells are vulnerable to excitotoxicity via specific glutamate receptors. Rapid desensitization of these receptors protects these cells from damage.
Area of Science:
- Neuroscience
- Cell Biology
- Neurochemistry
Background:
- Oligodendrocyte-like cells (OLC) express Ca2+-permeable glutamate receptors (GluR).
- Glutamate excitotoxicity is a significant concern in neurological conditions.
Purpose of the Study:
- To investigate the role of glutamate receptor subtypes in OLC excitotoxicity.
- To identify the specific GluR subunits involved in kainate-induced OLC damage.
Main Methods:
- Exposure of CG-4 derived OLC to kainate and AMPA.
- Assessment of Ca2+ influx, plasma membrane integrity, and DNA damage.
- Analysis of GluR mRNA and protein subunit expression.
Main Results:
- Kainate exposure caused Ca2+ influx, plasma membrane damage, and DNA nicking in OLC.
- AMPA blocked kainate-induced excitotoxicity, implicating AMPA-GluR.
- OLC excitotoxicity was mediated by AMPA-GluR containing flip GluR3 and/or flip GluR4 subunits, but not GluR2 subunits.
Conclusions:
- OLC excitotoxicity is mediated by specific AMPA-GluR subtypes.
- Rapid desensitization of these receptors is crucial for protecting oligodendroglial lineage cells.