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          Institute: MPI für medizinische Forschung     Collection: Abteilung Zellphysiologie     Display Documents

ID: 23075.0, MPI für medizinische Forschung / Abteilung Zellphysiologie
Inflammatory Mediators Potentiate ATP-gated Channels through the P2X3 Subunit
Translation of Title:Inflammatory Mediators Potentiate ATP-gated Channels through the P2X<SUB>3</SUB> Subunit
Authors:Paukert, Marti; Osteroth, Ralph; Geisler, Hyun-Soon; Brändle, Uwe; Glowatzki, Elisabeth; Ruppersberg, J. Peter; Gründer, Stefan
Date of Publication (YYYY-MM-DD):2001-06-15
Title of Journal:Journal of Biological Chemistry
Journal Abbrev.:J. Biol. Chem. (JBCHA3)
Issue / Number:24
Start Page:21077
End Page:21082
Review Status:Peer-review
Audience:Experts Only
Intended Educational Use:No
Abstract / Description:The P2X3 receptor is an ATP-gated ion channel predominantly expressed in nociceptive neurons from the dorsal root ganglion. P2X3 receptor channels are highly expressed in sensory neurons and probably contribute to the sensation of pain. Kinetics of P2X3 currents are characterized by rapid desensitization (<100 ms) and slow recovery (>20 s). Thus, any mechanism modulating rate of desensitization and/or recovery may have profound effect on susceptibility of nociceptive neurons expressing P2X3 to ATP. Here we show that currents mediated by P2X3 receptor channels and the heteromeric channel P2X2/3 composed of P2X2 and P2X3 subunits are potentiated by the neuropeptides substance P and bradykinin, which are known to modulate pain perception. The effect is mediated by the respective neuropeptide receptors, can be mimicked by phorbol ester and blocked by inhibitors of protein kinases. Together with data from site-directed mutagenesis our results suggest that inflammatory mediators sensitize nociceptors through phosphorylation of P2X3 and P2X2/3 ion channels or associated proteins.
External Publication Status:published
Document Type:Article
Communicated by:Wulf Kaiser
Affiliations:MPI für medizinische Forschung/Abteilung Zellphysiologie/
Identifiers:URI: [Full text]
URI: [Abstract]
URI: [Fulltext PDF]
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