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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 457079, 10 pages
Review Article

Kainic Acid-Induced Neurodegenerative Model: Potentials and Limitations

1Department of Neurosurgery, The First Hospital of Jilin University, Changchun 130021, China
2Department of Neurobiology, Care Science and Society, Karolinska Institute, Karolinska University Hospital Huddinge, SE-141 86 Stockholm, Sweden
3Department of Neurology, the First Hospital of Jilin University, Changchun 130021, China

Received 14 September 2010; Accepted 25 October 2010

Academic Editor: Monica Fedele

Copyright © 2011 Xiang-Yu Zheng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Excitotoxicity is considered to be an important mechanism involved in various neurodegenerative diseases in the central nervous system (CNS) such as Alzheimer's disease (AD). However, the mechanism by which excitotoxicity is implicated in neurodegenerative disorders remains unclear. Kainic acid (KA) is an epileptogenic and neuroexcitotoxic agent by acting on specific kainate receptors (KARs) in the CNS. KA has been extensively used as a specific agonist for ionotrophic glutamate receptors (iGluRs), for example, KARs, to mimic glutamate excitotoxicity in neurodegenerative models as well as to distinguish other iGluRs such as α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors and N-methyl-D-aspartate receptors. Given the current knowledge of excitotoxicity in neurodegeneration, interventions targeted at modulating excitotoxicity are promising in terms of dealing with neurodegenerative disorders. This paper summarizes the up-to-date knowledge of neurodegenerative studies based on KA-induced animal model, with emphasis on its potentials and limitations.