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

Abstract

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