Phosphatase inhibition prevents the activity-dependent trafficking of GABAAreceptors during status epilepticus in the young animal
Author:
Affiliation:
1. Department of Neurology; University of Virginia Health System; Charlottesville Virginia U.S.A
2. Department of Pediatrics; University of Virginia Health System; Charlottesville Virginia U.S.A
Funder
National Institute of Neurological Disorders and Stroke
American Academy of Neurology
Publisher
Wiley
Subject
Clinical Neurology,Neurology
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1111/epi.13098/fullpdf
Reference39 articles.
1. The impact of diazepam's discovery on the treatment and understanding of status epilepticus;Goodkin;Epilepsia,2009
2. Subunit-specific trafficking of GABAA receptors during status epilepticus;Goodkin;J Neurosci,2008
3. Trafficking of GABAA receptors, loss of inhibition, and a mechanism for pharmacoresistance in status epilepticus;Naylor;J Neurosci,2005
4. Deficits in phosphorylation of GABAA receptors by intimately associated protein kinase C activity underlie compromised synaptic inhibition during status epilepticus;Terunuma;J Neurosci,2008
5. Experimental status epilepticus alters GABAA receptor function in CA1 pyramidal neurons;Kapur;Ann Neurol,1995
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