Posttraumatic Epilepsy: Hemorrhage,Free Radicals and the Molecular Regulation of Glutamate |
| |
Authors: | L J Willmore Yuto Ueda |
| |
Institution: | (1) Department of Neurology & Psychiatry, Saint Louis University School of Medicine, 1402 South Grand Blvd. [M226], St. Louis, MI 63104, USA;(2) Department of Psychiatry, Miyazaki Medical College, Miyazaki, Japan |
| |
Abstract: | Traumatic brain injury causes development of posttraumatic epilepsy. Bleeding within neuropil is followed by hemolysis and
deposition of hemoglobin in neocortex. Iron from hemoglobin and transferring is deposited in brains of patients with posttraumatic
epilepsy. Iron compounds form reactive free radical oxidants. Microinjection of ferric ions into rodent brain results in chronic
recurrent seizures and liberation of glutamate into the neuropil, as is observed in humans with epilepsy. Termination of synaptic
effects of glutamate is by removal via transporter proteins. EAAC-1 is within neurons while GLT-1 and GLAST are confined to
glia. Persistent down regulation of GLAST production is present in hippocampal regions in chronic seizure models. Down regulation
of GLAST may be fundamental to a sequence of free radical reactions initiated by brain injury with hemorrhage. Administration
of antioxidants to animals causes interruption of the sequence of brain injury responses induced by hemorrhage, suggesting
that such a strategy needs to be evaluated in patients with traumatic brain injury.
Special issue article in honor of Dr. Akitane Mori. |
| |
Keywords: | Free radicals Peroxidation GLAST GLT-1 EAAC1 Transporter Ferric Epilepsy Glutamate Tocopherol |
本文献已被 PubMed SpringerLink 等数据库收录! |
|