ArticleMolecular pain2011
Cellular prion protein protects from inflammatory and neuropathic pain.
Article in Molecular pain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Multi-regional transcriptomic analysis reveals early nociceptive and neuroinflammatory alterations in APP/PS1 mice.Frontiers in immunology · 2026Article
- The role of cellular prion protein in immune system.BMB reports · 2023Review
- Development of an AmpliSeqFrontiers in pharmacology · 2018Article
- The biological function of the cellular prion protein: an update.BMC biology · 2017Review
- Physiological Functions of the Cellular Prion Protein.Frontiers in molecular biosciences · 2017Review
- Effect of the T-type channel blocker KYS-05090S in mouse models of acute and neuropathic pain.Pflugers Archiv : European journal of physiology · 2016Article
- Synthesis and characterization of a disubstituted piperazine derivative with T-type channel blocking action and analgesic properties.Molecular pain · 2016Article
- Analgesic effect of a broad-spectrum dihydropyridine inhibitor of voltage-gated calcium channels.Pflugers Archiv : European journal of physiology · 2015Article
- 1,4-Dihydropyridine derivatives with T-type calcium channel blocking activity attenuate inflammatory and neuropathic pain.Pflugers Archiv : European journal of physiology · 2015Article
- Glutamate receptors function as scaffolds for the regulation of β-amyloid and cellular prion protein signaling complexes.Molecular brain · 2015Review
- Characterization of novel cannabinoid based T-type calcium channel blockers with analgesic effects.ACS chemical neuroscience · 2015Article
- Cellular prion protein (PrP(C)) and its role in stress responses.International journal of clinical and experimental medicine · 2015Article
- Article
- Cellular prion protein and NMDA receptor modulation: protecting against excitotoxicity.Frontiers in cell and developmental biology · 2014Review
- Analgesic effect of a mixed T-type channel inhibitor/CB2 receptor agonist.Molecular pain · 2013Article
- Copper-dependent regulation of NMDA receptors by cellular prion protein: implications for neurodegenerative disorders.The Journal of physiology · 2012Review
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular prion protein (PrPC) inhibits N-Methyl-D-Aspartate (NMDA) receptors. Since NMDA receptors play an important role in the transmission of pain signals in the dorsal horn of spinal cord, we thus wanted to determine if PrPC null mice show a reduced threshold for various pain behaviours.We compared nociceptive thresholds between wild type and PrPC null mice in models of inflammatory and neuropathic pain, in the presence and the absence of a NMDA receptor antagonist. 2-3 months old male PrPC null mice exhibited an MK-801 sensitive decrease in the paw withdrawal threshold in response both mechanical and thermal stimuli. PrPC null mice also exhibited significantly longer licking/biting time during both the first and second phases of formalin-induced inflammation of the paw, which was again prevented by treatment of the mice with MK-801, and responded more strongly to glutamate injection into the paw. Compared to wild type animals, PrPC null mice also exhibited a significantly greater nociceptive response (licking/biting) after intrathecal injection of NMDA. Sciatic nerve ligation resulted in MK-801 sensitive neuropathic pain in wild-type mice, but did not further augment the basal increase in pain behaviour observed in the null mice, suggesting that mice lacking PrPC may already be in a state of tonic central sensitization. Altogether, our data indicate that PrPC exerts a critical role in modulating nociceptive transmission at the spinal cord level, and fit with the concept of NMDA receptor hyperfunction in the absence of PrPC.
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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.