ArticleNeuron2012
Mutant PrP suppresses glutamatergic neurotransmission in cerebellar granule neurons by impairing membrane delivery of VGCC α(2)δ-1 Subunit.
Article in Neuron, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
48 citing papers in PubMed, 69 citations in OpenAlex.
- Pregabalin Depresses Cerebellar Parallel Fiber-Purkinje Cell Synaptic Transmission by Modulating Glun2a-Containing Nmda Receptors in Mice In Vitro.International journal of molecular sciences · 2026Article
- Molecular Partners of Voltage-Gated Calcium Channel β and αThe Journal of membrane biology · 2026Review
- Roles of prion proteins in mammalian development.Animal cells and systems · 2024Review
- Prion propagation and cellular dysfunction in prion disease: Disconnecting the dots.PLoS pathogens · 2023Article
- A tetracationic porphyrin with dual anti-prion activity.iScience · 2023Article
- Prion Pathogenesis Revealed in a Series of the Special Issues "Prions and Prion Diseases".International journal of molecular sciences · 2022Article
- Endosomal sorting drives the formation of axonal prion protein endoggresomes.Science advances · 2021Article
- More than a pore: How voltage-gated calcium channels act on different levels of neuronal communication regulation.Channels (Austin, Tex.) · 2021Review
- Presynaptic αProceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Role of Cellular Prion Protein in Promoting Stemness and Differentiation in Cancer.Cancers · 2021Review
- PrPFrontiers in molecular neuroscience · 2021Review
- Cellular Prion Protein (PrPc): Putative Interacting Partners and Consequences of the Interaction.International journal of molecular sciences · 2020Review
- Neuronal αPflugers Archiv : European journal of physiology · 2020Review
- Mutant prion proteins increase calcium permeability of AMPA receptors, exacerbating excitotoxicity.PLoS pathogens · 2020Article
- Prion Protein in Glioblastoma Multiforme.International journal of molecular sciences · 2019Review
- The Prion Protein Regulates Synaptic Transmission by Controlling the Expression of Proteins Key to Synaptic Vesicle Recycling and Exocytosis.Molecular neurobiology · 2019Article
- CACHD1 is an α2δ-Like Protein That Modulates CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Induction of a transmissible tau pathology by traumatic brain injury.Brain : a journal of neurology · 2018Article
- Prions, prionoids and protein misfolding disorders.Nature reviews. Genetics · 2018Review
- Voltage-gated calcium channel αF1000Research · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
How mutant prion protein (PrP) leads to neurological dysfunction in genetic prion diseases is unknown. Tg(PG14) mice synthesize a misfolded mutant PrP which is partially retained in the neuronal endoplasmic reticulum (ER). As these mice age, they develop ataxia and massive degeneration of cerebellar granule neurons (CGNs). Here, we report that motor behavioral deficits in Tg(PG14) mice emerge before neurodegeneration and are associated with defective glutamate exocytosis from granule neurons due to impaired calcium dynamics. We found that mutant PrP interacts with the voltage-gated calcium channel α(2)δ-1 subunit, which promotes the anterograde trafficking of the channel. Owing to ER retention of mutant PrP, α(2)δ-1 accumulates intracellularly, impairing delivery of the channel complex to the cell surface. Thus, mutant PrP disrupts cerebellar glutamatergic neurotransmission by reducing the number of functional channels in CGNs. These results link intracellular PrP retention to synaptic dysfunction, indicating new modalities of neurotoxicity and potential therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.