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Brain Damage from Soman-Induced Seizures Is Greatly Exacerbated by Dimethyl sulfoxide (DMSO): Modest Neuroprotection by 2-Aminoethyl diphenylborinate (2-APB), a Transient Receptor Potential Channel Inhibitor and Inositol 1,4,5-triphosphate Receptor Antago

By Gerald P. H. Ballough, Robert K. Kan, James D. Nicholson, Denise M. Fath, Christina P. Tompkins, Gina M. Moffa and Margaret G. Filbert


The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Army or the Department of Defense. In conducting the research described in this report, the investigators complied with the regulations and standards of the Animal Welfare Act and adhered to the principles of the Guide for the Care and Use of Laboratory Animals (NRC 1996). The use of trade names does not constitute an official endorsement or approval of the use of such commercial hardware, software or pharmaceutical products. This document may not be cited for purposes of advertisement. Soman is a nerve-agent that produces seizures and seizure-related brain damage (SRBD). It is well known that termination of soman-induced seizures, using anticonvulsant drug therapy, would be the ideal means of preventing SRBD. However, these seizures quickly develop into status epilepticus and become refractory to anticonvulsant therapy shortly after their onset. Medical care for some battlefield casualties will likely be delayed beyond the therapeutic window of opportunity to terminate soman-induced seizures. Moreover, SRBD that has already been triggered wil

Year: 2008
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