Mitochondrial complex I inhibition produces selective damage to hippocampal subfield CA1 in organotypic slice cultures

Guangping Xu, Miguel A. Perez-Pinzon, Thomas J. Sick

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

The effects of mitochondrial respiratory chain inhibitors and the excitotoxin N-methyl-D-aspartate (NMDA) on cell death in hippocampal subfields CA1 and CA3 were examined in hippocampal organotypic slice cultures. Slice cultures, 2-3 week old, were exposed for 1 h to either the Complex 1 inhibitors, rotenone or 1-methyl-4-phenylpyridium (MPP+), the Complex II inhibitor 3-nitropropionic acid (3-NP), or the excitotoxin NMDA. Cell death was examined 24 and 48 h following treatment, by measuring propidium iodide (PI) fluorescence. Treatment with 1 μM rotenone caused greater cell death in hippocampal subfield CA1 than CA3. Exposure of hippocampal slice cultures to 10 μM rotenone, to MPP+ or to NMDA resulted in damage to both CA1 and CA3 subfields. 3-NP produced little damage in either subfield. The data suggest that mitochondrial complex I inhibition can produce selective cell damage in hippocampus and in this regard is similar to that observed following hypoxia/ischemia.

Original languageEnglish (US)
Pages (from-to)529-537
Number of pages9
JournalNeurotoxicity Research
Volume5
Issue number7
DOIs
StatePublished - Dec 1 2003

Keywords

  • Excitotoxicity
  • Mitochondrialtoxins
  • Selective neuronal vulnerability

ASJC Scopus subject areas

  • Neuroscience(all)
  • Toxicology

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