Kainic acid induced excitotoxicity

Milatovic D., Gupta R. C., and Dettbam W. D. (2002). Involvement of nitric oxide in kainic acid-induced excitotoxicity in rat brain. Brain Res. 957 330-337. 

Parihar M. S. and Hemnani T. (2003). Phenolic antioxidants attenuate hippocampal neuronal cell damage against kainic acid induced excitotoxicity. J. Biosci. 28 121-128. 

Neema M, Navarro-Quiroga I, Chechlacz M, Gilliams-Francis K, Liu J, et al. 2005. DNA damage and non-homologous end joining in excitotoxicity Neuroprotective role of DNA-pkcs in kainic acid-induced seizures. Hippocampus 15 1057-1071. 

IX. OXIDATIVE DAMAGE AND DENDRITIC DEGENERATION FOLLOWING KAINIC ACID-INDUCED EXCITOTOXICITY... 

Zaja-Milatovic, S., Gupta, R.C., Aschner, M., Montine, T.J., Milatovic, D. (2008). Pharmacologic suppression of oxidative damage and dendritic degeneration following kainic acid-induced excitotoxicity in mouse cerebrum. Neurotoxicology 29 621-7. 

Borlongan, C.V., Shytle, R.D., Ross, S.D., Shimizu, T., Freeman, T.B., Cahill, D.W., 1995. Nicotinic protects against systemic kainic acid-induced excitotoxic effects. Exp. Neurol. 136, 261-265. 

Ferrer I, Planas AM, Pozas E. Radiation-induced apoptosis in developing rats and kainic acid-induced excitotoxicity in adult rats are associated with distinctive morphological and biochemical c-Jun/AP-1 (N) expression. Neurosci 1997 80(2) 449 58. 

Stewart, G.R., Zorumski, C.E, Price, M.T., and Olney, J. W. 1990. Domoic acid a dementia-inducing excitotoxic food poison with kainic acid receptor specificity. xp 77euro/110, 127-138. 

Apoptotic/necrotic transformation of excitable cells. Effects of dipeptides directed to support stability of cellular structures increase the reliability of cellular functions under normal conditions and especially during oxidative stress, which accompanies effect of several extreme factors. It was found in experiments on individual neurons that carnosine prevents cell death induced by excitotoxic compounds, N-methyl-D-aspartic acid (NMDA) or kainate [93-95] or experimental hypoxia/reoxigenation [96]. Apoptosis induced by exposure of cerebellum neurons to kainic acid (see Table 6), was arrested if the cells were pre-incubated with carnosine or anserine and simultaneously heavy necrotic processes were substitute by light (reversible) necrosis. At the same time, N-acetylcamosine or homocaraosine did not reveal protecting action [94,95]. 

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