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

2015 | journal article. A publication with affiliation to the University of Göttingen.

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​Involvement of PrP(C) in kainate-induced excitotoxicity in several mouse strains.​
Carulla, P.; Llorens, F.; Matamoros-Angles, A.; Aguilar-Calvo, P.; Espinosa, J. C.; Gavín, R. & Ferrer, I. et al.​ (2015) 
Scientific reports5 art. 11971​.​ DOI: https://doi.org/10.1038/srep11971 

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Authors
Carulla, Patricia; Llorens, Franc; Matamoros-Angles, Andreu; Aguilar-Calvo, Patricia; Espinosa, Juan Carlos; Gavín, Rosalina; Ferrer, Isidre; Legname, Giuseppe; Torres, Juan Maria; Del Río, José A.
Abstract
The cellular prion protein (PrP(C)) has been associated with a plethora of cellular functions ranging from cell cycle to neuroprotection. Mice lacking PrP(C) 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 PrP(C) 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 Prnp(0/0) mice of B6129, B6.129, 129/Ola or FVB/N genetic backgrounds. Our study indicates that PrP(C) plays a role in neuroprotection in KA-treated cells and mice. For this function, PrP(C) should contain the aa32-93 region and needs to be linked to the membrane. In addition, some unidentified "Prnp-flanking genes" play a role parallel to PrP(C) in the KA-mediated responses in B6129 and B6.129 Prnp(0/0) mice.
Issue Date
2015
Journal
Scientific reports 
Project
info:eu-repo/grantAgreement/EC/FP7/222887/EU//PRIORITY
ISSN
2045-2322
Language
English

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