Impaired pain sensation in mice lacking prokineticin 2

• Main Authors: Amadesi Silvia, Luo Z David, Li Jia-Da, Zhang Chengkang, Hu Wang-Ping, Bunnett Nigel, Zhou Qun-Yong
• Format: Article
• Language: English
• Published: SAGE Publishing 2006-11-01
• Series: Molecular Pain
• Online Access: http://www.molecularpain.com/content/2/1/35

<p>Abstract</p> <p>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 <it>PK2 </it>gene displayed strong reduction in nociception induced by thermal and chemical stimuli, including capsaicin. However, <it>PK2 </it>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.</p>