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Related Concept Videos

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...

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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
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Glutamate receptor expression in multiple sclerosis lesions.

Jia Newcombe1, Alim Uddin, Rosamund Dove

  • 1Department of Neuroinflammation, Institute of Neurology, University College London, London, UK. J.Newcombe@ion.ucl.ac.uk

Brain Pathology (Zurich, Switzerland)
|October 11, 2007
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Summary

Glutamate excitotoxicity may contribute to multiple sclerosis (MS) pathogenesis. While astrocytes attempt to clear glutamate, increased glutamate receptor 1 (GluR1) on oligodendrocytes in MS lesions may cause excitotoxic damage.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Multiple sclerosis (MS) is a central nervous system (CNS) inflammatory demyelinating disease.
  • Blockade of glutamate receptors alleviates neurological signs in MS models.
  • The role of glutamate excitotoxicity in MS pathogenesis requires investigation.

Purpose of the Study:

  • To examine the cellular localization of glutamate, its receptors, transporters, and enzymes in active MS lesions.
  • To determine if glutamate excitotoxicity contributes to MS pathogenesis.

Main Methods:

  • Immunohistochemistry was used to detect glutamate, receptors (AMPA, NMdAR, kainate), transporters (GLT-1, EAAC1), and enzymes.
  • Cellular localization was assessed in active MS lesion borders, including oligodendrocytes, astrocytes, microglia, macrophages, endothelial cells, and axons.

Main Results:

  • Glutamate receptor 1 (GluR1), a Ca(++)-permeable AMPA subunit, was upregulated on oligodendrocytes in active MS lesions.
  • Reactive astrocytes expressed GluR3, mGluR1, 2/3, 5 receptors, GLT-1 transporter, and glutamate.
  • Microglia/macrophages showed GluR2, GluR4, and NMDA receptor subunit 1; endothelial cells and axons had kainate receptors (GluR5-7).
  • Astrocytes and macrophages expressed glutamate-metabolizing enzymes and the EAAC1 transporter.

Conclusions:

  • Reactive astrocytes in MS lesions possess mechanisms for glutamate sequestration and metabolism.
  • Upregulation of GluR1 on oligodendrocytes may render them vulnerable to excitotoxic damage.
  • Astrocytes may be unable to sufficiently reduce extracellular glutamate levels to protect oligodendrocytes in active MS lesions.