Excitotoxic mechanism

Avanzini, G (1992) Generalised epileptogenesis. In Epileptogenic and Excitotoxic Mechanisms (Eds Avanzini, G, Fariello, R, Heinemann, U and Mutani, R), John Libbey, London pp.29 0. 

Danysz W, Parsons CG, Mobius HJ, et al (2000) Neuroprotective and symptomatological action of memantine relevant for Alzheimer s disease—an unified glutamatergic hypothesis on the mechanism of action. Neurotox Res 2 85-97 Davis SM, Lees KR, Albers GW, et al (2000) Selfotel in acute ischemic stroke possible neurotoxic effects of an NMDA antagonist. Stroke 31 347-354 DeKeyser J (1991) Excitotoxic mechanisms may be involved in the pathophysiology of tardive dyskinesia. Clin Neuropharmacol 14 562-565 Del Dotto P, Pavese N, Gambaccini G, et al (2001) Intravenous amantadine improves levodopa-induced dyskinesias an acute double-blind placebo-controlled study. Mov Disord 16 515-520... 

Yi J. H. and Hazell A. S. (2006). Excitotoxic mechanisms and the role of astrocytic glutamate transporters in traumatic brain injury. Neurochem. Int. 48 394 103. 

Castillo J., Davalos A., and Noya M. (1999) Aggravation of acute ischemic stroke by hyperthermia is related to an excitotoxic mechanism. Cerebrovasc. Dis. 9, 22-27. 

Auer, R.N. 1991. Excitotoxic mechanisms, and age-related susceptibility to brain damage in ischemia, hypoglycemia and toxic mussel poisoning. Neurotoxicology 12, 541-546. 

Hazell, A.S. (2007). Excitotoxic mechanisms in stroke an update of concepts and treatment strategies. Neurochem. Int. 50 941-53. 

Long term activation of glutamate receptors taking place during disordering of neuronal function is a factor, which can result in cell death. Excitotoxic mechanisms of cell death are... 

Although the exact cause of the progressive degeneration of nigrostriatal dopamine neurons in Parkinson s disease is still unknown, several mechanisms were proposed to explain the cell damaging processes at the molecular level that ultimately cause Parkinson s disease.127 These mechanisms, which are probably related by interacting mechanisms, include (1) excitotoxic mechanism, (2) mitochondrial toxins, and (3) oxidative stress. 

Fig. 1.2 Putative cascade of damaging events in focal cerebral ischemia. Very early after the onset of the focal perfusion deficit, excitotoxic mechanisms can damage neurones and glia lethaUy. In addition, excitotoxicity triggers a number of events that can further contribute to the demise of the tissue. Such events include peri-infarct depolarizations and the more-delayed mechanisms of inflammation and programmed cell death. The x-axis reflects the evolution of the cascade over time, while the y-axis aims to illustrate the impact of each element of the cascade on final outcome (courtesy of Dimagl et al. 1999)...

Hypoglycemia may be summarized as a novel insult that has a number of features unsuspected several decades ago. These include a positive, excitotoxic mechanism of neuronal death, not merely nenronal death by starvation. Asymmetry is sometimes seen, and is explained by the asynchronous onset of electrocerebral silence between the hemispheres. And selective necrosis of the dentate gyrus is not seen in cerebral ischemia, the dentate being the last structure within the hippocampus to be destroyed by ischemia. Based on these principles, it is sometimes possible to tell hypoglycemic from ischemic brain damage in human brains. 

Post-synaptic receptors are also altered in the brain of patients with Alzheimer s disease. NMDA and metabotropic receptors are decreased with less marked effects on AMPA receptors. These changes occur in areas of the brain most pathologically affected by the disease. Several pieces of evidence are inconsistent with a primary role for excitotoxic mechanisms in the aetiology of Alzheimer s disease, but it is nevertheless probable that these mechanisms participate in the pathogenesis of Alzheimer s disease which explains the development of many compounds affecting all levels of aminoexcitatory transmission. 

J. D. Rothstein. Excitotoxic mechanisms in the pathogenesis of amyotrophic lateral sclerosis. Adv.Neurol. 68 7-20,1995. 

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