Antioxidant NAC and AMPA/KA receptor antagonist DNQX inhibited JNK3 activation following global ischemia in rat hippocampus

Neuroscience Research
Hui TianQuanguang Zhang

Abstract

c-Jun N-terminal kinase-3 (JNK3), the only neural-specific isoform, may play an important role in excitotoxicity and neuronal injury. To analyze the variation of JNK3 activation, levels of phospho-JNK3 were measured at various time points of ischemia and selected time points of reperfusion, respectively. Our study illustrated that JNK3 was rapidly activated and translocated from cytosol to nucleus during ischemia. During reperfusion, two peaks of JNK3 activation occurred at 30 min and 3 days, respectively. To further define the mechanism of JNK3 activation, antioxidant N-acetylcysteine (NAC), alpha-amino-3-hydroxyl-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate (KA) receptor antagonist 6,7-dinitro-quinoxaline-2,3(1H,4H)-dione (DNQX), N-methyl-D-aspartate (NMDA) receptor antagonist ketamine and L-type voltage-gated Ca(2+) channel (L-VGCC) antagonist nifedipine were given to the rats 20 min prior to ischemia. The results showed that NAC obviously inhibited JNK3 activation during the early reperfusion, whereas DNQX preferably attenuated JNK3 activation during the latter reperfusion. Ketamine and nifedipine had no significant effects on JNK3 activation during reperfusion. Consequently, reactive oxygen species (ROS) and AMPA/KA r...Continue Reading

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Citations

Jul 3, 2010·Science China. Life Sciences·YiZheng Wang, TianLe Xu
Jan 28, 2005·The European Journal of Neuroscience·Stephan BrechtThomas Herdegen
Sep 30, 2014·Journal of Receptor and Signal Transduction Research·Zhen-Zhen DuanQi Su-Hua
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Jan 7, 2006·Journal of Neuroscience Research·Deborah A Shackelford, Richard Y Yeh
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Jul 12, 2005·Molecular and Cellular Neurosciences·Vicki Waetzig, Thomas Herdegen

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