| First Author | Khasar SG | Year | 1999 |
| Journal | Neuron | Volume | 24 |
| Issue | 1 | Pages | 253-60 |
| PubMed ID | 10677042 | Mgi Jnum | J:57887 |
| Mgi Id | MGI:1345916 | Doi | 10.1016/s0896-6273(00)80837-5 |
| Citation | Khasar SG, et al. (1999) A novel nociceptor signaling pathway revealed in protein kinase C epsilon mutant mice. Neuron 24(1):253-60 |
| abstractText | There is great interest in discovering new targets for pain therapy since current methods of analgesia are often only partially successful. Although protein kinase C (PKC) enhances nociceptor function, it is not known which PKC isozymes contribute. Here, we show that epinephrine-induced mechanical and thermal hyperalgesia and acetic acid-associated hyperalgesia are markedly attenuated in PKCepsilon mutant mice, but baseline nociceptive thresholds are normal. Moreover, epinephrine-, carrageenan-, and nerve growth factor- (NGF-) induced hyperalgesia in normal rats, and epinephrine-induced enhancement of tetrodotoxin-resistant Na+ current (TTX-R I(Na)) in cultured rat dorsal root ganglion (DRG) neurons, are inhibited by a PKCepsilon-selective inhibitor peptide. Our findings indicate that PKCepsilon regulates nociceptor function and suggest that PKCepsilon inhibitors could prove useful in the treatment of pain. |
