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Autor/inn/enWoldbye, David P. D.; Angehagen, Mikael; Gotzsche, Casper R.; Elbrond-Bek, Heidi; Sorensen, Andreas T.; Christiansen, Soren H.; Olesen, Mikkel V.; Nikitidou, Litsa; Hansen, Thomas v. O.; Kanter-Schlifke, Irene; Kokaia, Merab
TitelAdeno-Associated Viral Vector-Induced Overexpression of Neuropeptide Y Y2 Receptors in the Hippocampus Suppresses Seizures
QuelleIn: Brain, 133 (2010) 9, S.2778-2788 (11 Seiten)
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Spracheenglisch
Dokumenttypgedruckt; online; Zeitschriftenaufsatz
ISSN0006-8950
DOI10.1093/brain/awq219
SchlagwörterReading Difficulties; Epilepsy; Seizures; Phonemic Awareness; Patients; Reading Skills; Brain Hemisphere Functions; Genetics; Therapy; Biochemistry; Prevention
AbstractGene therapy using recombinant adeno-associated viral vectors overexpressing neuropeptide Y in the hippocampus exerts seizure-suppressant effects in rodent epilepsy models and is currently considered for clinical application in patients with intractable mesial temporal lobe epilepsy. Seizure suppression by neuropeptide Y in the hippocampus is predominantly mediated by Y2 receptors, which, together with neuropeptide Y, are upregulated after seizures as a compensatory mechanism. To explore whether such upregulation could prevent seizures, we overexpressed Y2 receptors in the hippocampus using recombinant adeno-associated viral vectors. In two temporal lobe epilepsy models, electrical kindling and kainate-induced seizures, vector-based transduction of Y2 receptor complementary DNA in the hippocampus of adult rats exerted seizure-suppressant effects. Simultaneous overexpression of Y2 and neuropeptide Y had a more pronounced seizure-suppressant effect. These results demonstrate that overexpression of Y2 receptors (alone or in combination with neuropeptide Y) could be an alternative strategy for epilepsy treatment. (As Provided).
AnmerkungenOxford University Press. Great Clarendon Street, Oxford, OX2 6DP, UK. Tel: +44-1865-353907; Fax: +44-1865-353485; e-mail: jnls.cust.serv@oxfordjournals.org; Web site: http://brain.oxfordjournals.org/
Erfasst vonERIC (Education Resources Information Center), Washington, DC
Update2017/4/10
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