Excitotoxicity in glial cells

Eur J Pharmacol. 2002 Jul 5;447(2-3):239-46. doi: 10.1016/s0014-2999(02)01847-2.

Abstract

Excitotoxicity results from prolonged activation of glutamate receptors expressed by cells in the central nervous system (CNS). This cell death mechanism was first discovered in retinal ganglion cells and subsequently in brain neurons. In addition, it has been recently observed that CNS glial cells can also undergo excitotoxicity. Among them, oligodendrocytes are highly vulnerable to glutamate signals and alterations in glutamate homeostasis may contribute to demyelinating disorders. We review here the available information on excitotoxity in CNS glial cells and its putative relevance to glio-pathologies.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amino Acid Transport System X-AG / physiology
  • Animals
  • Apoptosis*
  • Astrocytes / pathology
  • Calcium / metabolism
  • Glutamic Acid / toxicity*
  • Homeostasis
  • Humans
  • Microglia / pathology*
  • Neurodegenerative Diseases / etiology*
  • Oligodendroglia / pathology
  • Receptors, Glutamate / physiology*

Substances

  • Amino Acid Transport System X-AG
  • Receptors, Glutamate
  • Glutamic Acid
  • Calcium