Postsynaptic mechanisms of excitotoxicity: Involvement of postsynaptic density proteins, radicals, and oxidant molecules

Division of Fundamental Neurobiology, University Health Network, Toronto, Ontario, Canada M5T 2S8.
Neuroscience (Impact Factor: 3.36). 12/2008; 158(1):293-300. DOI: 10.1016/j.neuroscience.2008.10.021
Source: PubMed


Traditional models of neuronal excitotoxicity focused on the overactivation of receptors such as the ionotropic N-methyl-D-aspartate (NMDA)-subtype glutamate receptor. Recent developments have shifted focus to downstream neurotoxic signaling molecules with exciting implications to specific strategies for treating excitotoxic disorders. This review outlines these developments and introduces newly emerging evidence implicating the involvement of the melastatin subfamily in anoxic neuronal death. Both of these converge on the production of reactive oxygen species (ROS), including superoxide, nitric oxide (NO) and the oxidant peroxynitrite.

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Available from: Joan Forder, Nov 05, 2015
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    • ", 2003 ] , что приводит к сее рьезным нарушениям его развития . При кислоо родном голодании высвобождается значительь ное количество провоспалительных цитокии нов , и активных форм кислорода , реализуются механизмы эксайтотоксичности [ Forder , Tymianski , 2009 ] . Кроме того , при воспалии тельных реакциях усиливается активация гии поталамоогипофизарной надпочечниковой системы , которая ведет к увеличению высвоо бождения глюкокортикостероидов . "
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