Activation of ERK5 is mediated by N-methyl-D-aspartate receptor and L-type voltage-gated calcium channel via Src involving oxidative stress after cerebral ischemia in rat hippocampus

Rui Min Wang, Quan Guang Zhang, Guang Yi Zhang

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

Activation (phosphorylation) and the possible mechanism of extracellular signal-regulated kinase 5 (ERK5) were evaluated after cerebral ischemia-reperfusion (I/R) in the hippocampus in a four-vessel occlusion model of Sprague-Dawley rats. Western blotting showed that ERK5 was strongly activated from 10 min to 1 day and peaked at 30 min of reperfusion after 15 min ischemia. Pretreatment with N-acetylcysteine, a free radical scavenger, effectively inhibited ERK5 activation in a dose-dependent manner. Consistently, ERK5 activation was significantly suppressed by genistein (protein-tyrosine kinase inhibitor), PP2 (specific inhibitor of Src family kinases), nifedipine (L-VGCC blocker) and dextromethorphan (NMDA receptor antagonist), but not 6,7-dinitroquinoxaline-2, 3(1H, 4H)-dione (AMPA receptor antagonist). These results suggested that ERK5 could be significantly activated by I/R, which might be mediated by NMDA receptor and L-VGCC through Src kinase pathway involving oxidative stress in rat hippocampus.

Original languageEnglish (US)
Pages (from-to)13-16
Number of pages4
JournalNeuroscience Letters
Volume357
Issue number1
DOIs
StatePublished - Feb 26 2004
Externally publishedYes

Keywords

  • Activation
  • Cerebral ischemia
  • Extracellular signal-regulated kinase 5
  • Hippocampus
  • N-acetylcysteine
  • N-methyl-D-aspartate receptor
  • Rat
  • Src

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Activation of ERK5 is mediated by N-methyl-D-aspartate receptor and L-type voltage-gated calcium channel via Src involving oxidative stress after cerebral ischemia in rat hippocampus'. Together they form a unique fingerprint.

  • Cite this