A sublethal dose of TNFα potentiates kainate-induced excitotoxicity in optic nerve oligodendrocytes

Brandon A. Miller, Fang Sun, Randolph N. Christensen, Adam R. Ferguson, Jacqueline C. Bresnahan, Michael S. Beattie

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Glutamate receptor-induced cell death, known as excitotoxicity in both neurons and oligodendrocytes, has been implicated as a common pathway of cell death in numerous central nervous system (CNS) diseases and trauma. Research in both neuronal and oligodendrocyte excitotoxicity has examined glutamate's receptor-mediated effects on CNS cells, and explored strategies to protect cells exposed to the elevated glutamate levels that occur in CNS trauma and disease. Proinflammatory cytokines are also elevated in the injured CNS, and have also been implicated in CNS cell death. Recently, several laboratories have examined cytokines' effects on neuronal and glial excitotoxicity. Here, we review literature concerning the dynamic susceptibility of both neurons and oligodendrocytes to excitotoxicity, and present new data from our laboratory showing that the susceptibility of oligodendrocytes to excitotoxicity is acutely potentiated by the proinflammatory cytokine TNFα.

Original languageEnglish
Pages (from-to)867-875
Number of pages9
JournalNeurochemical Research
Issue number6-7
StatePublished - Jun 2005

Bibliographical note

Funding Information:
The authors thank John Komon for assistance preparing figures, and C. Amy Tovar and Dr. Mark Noble for their assistance with cell culture. This project was funded by NIH grant NS 38079.


  • AMPA
  • Excitotoxicity
  • Glutamate
  • Oligodendrocyte
  • TNFα

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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