The prion protein is required for normal responses to light stimuli by photoreceptor and bipolar cells
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ABSTRACT: The prion protein, PrPC, is well known as an essential susceptibility factor for neurodegenerative prion diseases, yet its function in normal, healthy cells remains uncertain. A role in synaptic function has been proposed for PrPC, supported by its cell surface expression in neurons and glia. Here, in mouse retina, we localized PrPC with synaptic proteins EAAT5, CtBP2 and PSD-95, which are present at junctions between photoreceptors and bipolar cells. PrPC localized most densely with the bipolar cell dendrites synapsing with cone photoreceptor terminals. In two coisogenic mouse strains, deletion of the gene encoding PrPC, Prnp, significantly altered the scotopic and photopic electroretinographic (ERG) responses of photoreceptor and bipolar cells. Cone-dominant pathways showed the most significant ERG changes. Retinal thickness, quantitated by high-resolution optical coherence tomography (OCT), and ribbon synapse morphology were not altered upon deletion of PrPC, suggesting that the ERG changes were driven by functional rather than structural alterations
ORGANISM(S): Mus musculus
PROVIDER: GSE264257 | GEO | 2024/10/16
REPOSITORIES: GEO
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