Neurochemical Research

, Volume 19, Issue 12, pp 1557–1564

Oxidative mechanisms involved in kainate-induced cytotoxicity in cortical neurons

  • Yu Cheng
  • Albert Y. Sun
Original Articles

DOI: 10.1007/BF00969006

Cite this article as:
Cheng, Y. & Sun, A.Y. Neurochem Res (1994) 19: 1557. doi:10.1007/BF00969006


In our previous experiments, evidence of free radical formation has been demonstrated in gerbil brain after kainic acid (KA) administration. In the present study, the mechanisms involved in KA-induced free radical formation and subsequent cell degeneration were investigated using high density cortical neuron cultures. A free radical trapping agent,a-phenyl-N-tert-butyl-nitrone (PBN), as well as the combined action of superoxide dismutase and catalase attenuated KA neurotoxic effect. Calpain-induced xanthine oxidase (XO) activation may play an important role in KA excitotoxicity since calpain inhibitor I as well as allopurinol, a selective XO inhibitor, significantly protected the cortical neurons from KA-induced cell death. However, XO activation may not be the only source producing free radicals, other free radical generating systems such as nitric oxide synphase may also play a role in KA insult.

Key Words

Free radicals kainic acid cortical neuron a-phenyl-N-tert-butyl-nitrone excitotoxicity xanthine oxidase 

Copyright information

© Plenum Publishing Corporation 1994

Authors and Affiliations

  • Yu Cheng
    • 1
  • Albert Y. Sun
    • 1
  1. 1.Department of PharmacologyUniversity of Missouri-Columbia School of MedicineColumbia