ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
PrPC controls via protein kinase A the direction of synaptic plasticity in the immature hippocampus.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- PrPEnvironmental science & technology · 2026Article
- Creutzfeldt-Jakob Disease Mimicking Transient Brain Ischemia in a Patient with a Mitral Valve Prosthesis-A Case Report.Reports (MDPI) · 2025Article
- Comparing Prion Proteins Across Species: Is Zebrafish a Useful Model?Molecular neurobiology · 2025Review
- Copper coordination modulates prion conversion and infectivity in mammalian prion proteins.Prion · 2023Review
- Structural and dynamical determinants of a β-sheet-enriched intermediate involved in amyloid fibrillar assembly of human prion protein.Chemical science · 2022Article
- Loss of prion protein control of glucose metabolism promotes neurodegeneration in model of prion diseases.PLoS pathogens · 2021Article
- Study on the Correlation Between NF-κB and Central Fatigue.Journal of molecular neuroscience : MN · 2021Review
- Mutations of CNTNAP1 led to defects in neuronal development.JCI insight · 2020Article
- Impairment of cerebellar long-term depression and GABAergic transmission in prion protein deficient mice ectopically expressing PrPLP/Dpl.Scientific reports · 2020Article
- Single-nucleus transcriptomics of the prefrontal cortex in major depressive disorder implicates oligodendrocyte precursor cells and excitatory neurons.Nature neuroscience · 2020Article
- Copper Binding Regulates Cellular Prion Protein Function.Molecular neurobiology · 2019Article
- Mutations Alter RNA-Mediated Conversion of Human Prions.ACS omega · 2018Article
- Elucidating the function of the prion protein.PLoS pathogens · 2017Review
- Molecular dynamics simulations of early steps in RNA-mediated conversion of prions.Protein science : a publication of the Protein Society · 2017Article
- Role of amyloid β protein receptors in mediating synaptic plasticity.Biomedical reports · 2017Article
- The N Terminus of the Prion Protein Mediates Functional Interactions with the Neuronal Cell Adhesion Molecule (NCAM) Fibronectin Domain.The Journal of biological chemistry · 2016Article
- Article
- Cellular prion protein promotes post-ischemic neuronal survival, angioneurogenesis and enhances neural progenitor cell homing via proteasome inhibition.Cell death & disease · 2015Article
- The non-octarepeat copper binding site of the prion protein is a key regulator of prion conversion.Scientific reports · 2015Article
- Prion Protein Modulates Monoaminergic Systems and Depressive-like Behavior in Mice.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cellular form of prion protein PrP(C) is highly expressed in the brain, where it can be converted into its abnormally folded isoform PrP(Sc) to cause neurodegenerative diseases. Its predominant synaptic localization suggests a crucial role in synaptic signaling. Interestingly, PrP(C) is developmentally regulated and its high expression in the immature brain could be instrumental in regulating neurogenesis and cell proliferation. Here, PrP(C)-deficient (Prnp(0/0)) mice were used to assess whether the prion protein is involved in synaptic plasticity processes in the neonatal hippocampus. To this aim, calcium transients associated with giant depolarizing potentials, a hallmark of developmental networks, were transiently paired with mossy fiber activation in such a way that the two events were coincident. While this procedure caused long-term potentiation (LTP) in wild-type (WT) animals, it caused long-term depression (LTD) in Prnp(0/0) mice. Induction of LTP was postsynaptic and required the activation of cAMP-dependent protein kinase A (PKA) signaling. The induction of LTD was presynaptic and relied on G-protein-coupled GluK1 receptor and protein lipase C. In addition, at emerging CA3-CA1 synapses in WT mice, but not in Prnp(0/0) mice, pairing Schaffer collateral stimulation with depolarization of CA1 principal cells induced LTP, known to be PKA dependent. Postsynaptic infusion of a constitutively active isoform of PKA catalytic subunit Cα into CA1 and CA3 principal cells in the hippocampus of Prnp(0/0) mice caused a persistent synaptic facilitation that was occluded by subsequent pairing. These data suggest that PrP(C) plays a crucial role in regulating via PKA synaptic plasticity in the developing hippocampus.
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