ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Alterations in Ca2+-buffering in prion-null mice: association with reduced afterhyperpolarizations in CA1 hippocampal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 29 citations in OpenAlex.
- The biological function of the cellular prion protein: an update.BMC biology · 2017Review
- Prion protein "gamma-cleavage": characterizing a novel endoproteolytic processing event.Cellular and molecular life sciences : CMLS · 2016Article
- Reduced Hyperpolarization-Activated Current Contributes to Enhanced Intrinsic Excitability in Cultured Hippocampal Neurons from PrP(-/-) Mice.Frontiers in cellular neuroscience · 2016Article
- The prion protein modulates A-type K+ currents mediated by Kv4.2 complexes through dipeptidyl aminopeptidase-like protein 6.The Journal of biological chemistry · 2013Article
- Prion protein and its role in signal transduction.Cellular & molecular biology letters · 2013Review
- Hippocalcin and KCNQ channels contribute to the kinetics of the slow afterhyperpolarization.Biophysical journal · 2012Article
- Bidirectional pattern-specific plasticity of the slow afterhyperpolarization in rats: role for high-voltage activated Ca2+ channels and I h.The European journal of neuroscience · 2011Article
- Article
- Enhanced calcium buffering in F344 rat cholinergic basal forebrain neurons is associated with age-related cognitive impairment.Journal of neurophysiology · 2009Article
- Endogenous calcium buffering capacity of substantia nigral dopamine neurons.Journal of neurophysiology · 2009Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Prion protein (PrP) is a normal component of neurons, which confers susceptibility to prion diseases. Despite its evolutionary conservation, its normal function remains controversial. PrP-deficient (Prnp(0/0)) mice have weaker afterhyperpolarizations (AHPs) in cerebellar and hippocampal neurons. Here we show that the AHP impairment in hippocampal CA1 pyramidal cells is selective for the slow AHP, and is not caused by an impairment of either voltage-gated Ca(2+) channels or Ca(2+)-activated K(+) channels. Instead, Prnp(0/0) neurons have twofold to threefold stronger Ca(2+) buffering and double the Ca(2+) extrusion rate. In Prnp(0/0) neurons thapsigargin abolished the stronger Ca(2+) buffering and extrusion, and thapsigargin or cyclopiazonic acid abolished the weakening of the slow AHPs. These data implicate sarcoplasmic/endoplasmic reticulum calcium ATPase in the enhanced Ca(2+) buffering, and extrusion into the endoplasmic reticulum, which contains substantial amounts of PrP in wild-type mice. Altered Ca(2+) homeostasis can explain several phenotypes identified in Prnp(0/0) mice.
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Registered trials
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