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    Impaired pain sensation in mice lacking prokineticin 2

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    43
    Author
    Hu, W-P; Zhang, C; Li, J-D; Luo, ZD; Amadesi, S; Bunnett, N; Zhou, Q-Y
    Date
    2006-11-15
    Source Title
    Molecular Pain
    Publisher
    BIOMED CENTRAL LTD
    University of Melbourne Author/s
    Bunnett, Nigel
    Affiliation
    Pharmacology and Therapeutics
    Metadata
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    Document Type
    Journal Article
    Citations
    Hu, W. -P., Zhang, C., Li, J. -D., Luo, Z. D., Amadesi, S., Bunnett, N. & Zhou, Q. -Y. (2006). Impaired pain sensation in mice lacking prokineticin 2. MOLECULAR PAIN, 2, https://doi.org/10.1186/1744-8069-2-35.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259465
    DOI
    10.1186/1744-8069-2-35
    Abstract
    Prokineticins (PKs), consisting of PK1 and PK2, are a pair of newly identified regulatory peptides. Two closely related G-protein coupled receptors, PKR1 and PKR2, mediate the signaling of PKs. PKs/PKRs participate in the regulation of diverse biological processes, ranging from development to adult physiology. A number of studies have indicated the involvement of PKs/PKRs in nociception. Here we show that PK2 is a sensitizer for nociception. Intraplantar injection of recombinant PK2 resulted in a strong and localized hyperalgesia with reduced thresholds to nociceptive stimuli. PK2 mobilizes calcium in dissociated dorsal root ganglion (DRG) neurons. Mice lacking the PK2 gene displayed strong reduction in nociception induced by thermal and chemical stimuli, including capsaicin. However, PK2 mutant mice showed no difference in inflammatory response to capsaicin. As the majority of PK2-responsive DRG neurons also expressed transient receptor potential vanilloid (TRPV1) and exhibited sensitivity to capsaicin, TRPV1 is likely a significant downstream molecule of PK2 signaling. Taken together, these results reveal that PK2 sensitize nociception without affecting inflammation.

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