Posttraumatic Epilepsy: Hemorrhage, Free Radicals and the Molecular Regulation of Glutamate
作者： L. J. Willmore , Yuto Ueda
DOI: 10.1007/S11064-008-9841-3
关键词: Hippocampal formation 、 Neocortex 、 Neuroscience 、 Endocrinology 、 Epilepsy 、 Neurology 、 Traumatic brain injury 、 Epileptogenesis 、 Glutamate receptor 、 Neuropil 、 Internal medicine 、 Chemistry
摘要: Traumatic brain injury causes development of posttraumatic epilepsy. Bleeding within neuropil is followed by hemolysis and deposition hemoglobin in neocortex. Iron from transferring deposited brains patients with compounds form reactive free radical oxidants. Microinjection ferric ions into rodent results chronic recurrent seizures liberation glutamate the neuropil, as observed humans Termination synaptic effects removal via transporter proteins. EAAC-1 neurons while GLT-1 GLAST are confined to glia. Persistent down regulation production present hippocampal regions seizure models. Down may be fundamental a sequence reactions initiated hemorrhage. Administration antioxidants animals interruption responses induced hemorrhage, suggesting that such strategy needs evaluated traumatic injury.
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