| First Author | Su YS | Year | 2016 |
| Journal | J Mol Neurosci | Volume | 59 |
| Issue | 1 | Pages | 113-25 |
| PubMed ID | 26635025 | Mgi Jnum | J:268774 |
| Mgi Id | MGI:6273277 | Doi | 10.1007/s12031-015-0693-4 |
| Citation | Su YS, et al. (2016) Serotonin Receptor 2B Mediates Mechanical Hyperalgesia by Regulating Transient Receptor Potential Vanilloid 1. J Mol Neurosci 59(1):113-25 |
| abstractText | Serotonin [5-hydroxytryptamine (5-HT)], an inflammatory mediator, contributes to inflammatory pain. The presence of multiple 5-HT subtype receptors on peripheral and central nociceptors complicates the role of 5-HT in pain. Previously, we found that 5-HT2B/2C antagonist could block 5-HT-induced mechanical hyperalgesia. However, the types of neurons or circuits underlying this effect remained unsolved. Here, we demonstrate that the Gq/11-phospholipase Cbeta-protein kinase Cepsilon (PKCepsilon) pathway mediated by 5-HT2B is involved in 5-HT-induced mechanical hyperalgesia in mice. Administration of a transient receptor potential vanilloid 1 (TRPV1) antagonist inhibited the 5-HT-induced mechanical hyperalgesia. 5-HT injection enhanced 5-HT- and capsaicin-evoked calcium signals specifically in isolectin B4 (IB4)-negative neurons; signals were inhibited by a 5-HT2B/2C antagonist and PKCepsilon blocker. Thus, 5-HT2B mediates 5-HT-induced mechanical hyperalgesia by regulating TRPV1 function. |
