Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9989738 | Neurobiology of Disease | 2005 | 11 Pages |
Abstract
Prion protein (PrPC) is a constituent of most normal mammalian cells and plays an essential role in the pathogenesis of transmissible spongiform encephalopathies (TSE). However, the normal cellular function of PrPC remains unclear. Here, we document that mice with a selective deletion of PrPC exhibited deficits in hippocampal-dependent spatial learning, but non-spatial learning remained intact. mPrPâ/â mice also showed reduction in paired-pulse facilitation and long-term potentiation in the dentate gyrus in vivo. These deficits were rescued in transgenic mPrPâ/â mice expressing PrPC in neurons under control of the neuron-specific enolase (NSE) promoter indicating that they were due to lack of PrPC function in neurons. The deficits were seen in mPrPâ/â mice with a homogeneous 129/Ola background and in mPrPâ/â mice in the mixed (129/Ola à C57BL/10) background indicating that these abnormalities were unlikely due to variability of background genes or alteration of the nearby Prnd (doppel) gene.
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Authors
José R. Criado, Manuel Sánchez-Alavez, Bruno Conti, Jeannie L. Giacchino, Derek N. Wills, Steven J. Henriksen, Richard Race, Jean C. Manson, Bruce Chesebro, Michael B.A. Oldstone,