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Seizures excitotoxicity

Neuronal excitotoxicity AEA levels are elevated in the hippocampus of mice treated with kainic acid. 2-AG levels are elevated in rats treated with pilocarpine These are two animal models of epileptic seizures, where the endocannabinoids play an anti-convulsant and protective function Inhibitors of cellular re-uptake... [Pg.467]

Excitotoxicity is the over-activity of the glutamatergic system responsible for the large number of dead neurons observed after ischemia (stroke) or epileptic seizures. This neuronal death is due to an overexcitation of the neurons and the massive Ca2+ entry... [Pg.487]

De Bock F., Dornand J., and Rondouin G. (1996). Release of TNFalpha in the rat hippocampus following epileptic seizures and excitotoxic neuronal damage. NeuroReport 7 1125-1129. [Pg.192]

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. [Pg.233]

Time-course changes in biomarkers of oxidative damage in the rat model of anticholinesterase-induced seizures showed that the highest increase in F2-IS0PS was evaluated at 1 h after the injection of anticholinesterase agent or 40 min after the beginning of seizure symptoms (Gupta et ah, 2007). In the model of KA-induced excitotoxicity the... [Pg.641]

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Excitotoxic

Excitotoxicity

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