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Involvement of PrP(C) in kainate-induced excitotoxicity in several mouse strains.

By Patricia Carulla Martí, Franc Llorens Torres, Andreu Matamoros-Anglès, Patricia Aguilar-Calvo, Juan Carlos Espinosa, Rosalina Gavín Marín, Isidro (Ferrer Abizanda) Ferrer, Giuseppe Legname, Juan María Torres and José Antonio del Río

Abstract

The cellular prion protein (PrPC) has been associated with a plethora of cellular functions ranging from cell cycle to neuroprotection. Mice lacking PrPC show an increased susceptibility to epileptic seizures; the protein, then, is neuroprotective. However, lack of experimental reproducibility has led to considering the possibility that other factors besides PrPC deletion, such as the genetic background of mice or the presence of so-called "Prnp flanking genes", might contribute to the reported susceptibility. Here, we performed a comparative analysis of seizure-susceptibility using characterized Prnp+/+ and Prnp0/0 mice of B6129, B6.129, 129/Ola or FVB/N genetic backgrounds. Our study indicates that PrPC plays a role in neuroprotection in KA-treated cells and mice. For this function, PrPC should contain the aa32<br>93 region and needs to be linked to the membrane. In addition, some unidentified "Prnp-flanking genes" play a role parallel to PrPC in the KA-mediated responses in B6129 and B6.129 Prnp0/0 mice

Topics: Malalties del sistema nerviós, Neurociències, Nervous System Diseases, Neurosciences
Publisher: Nature Publishing Group
Year: 2015
DOI identifier: 10.1038/srep11971
OAI identifier: oai:diposit.ub.edu:2445/66627
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