| Autor: |
Su, Yeu-Shiuan, Chiu, Yuan-Yi, Lin, Shih-Yuan, Chen, Chih-Cheng, Sun, Wei-Hsin |
| Zdroj: |
Journal of Molecular Neuroscience; May2016, Vol. 59 Issue 1, p113-125, 13p |
| Abstrakt: |
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-HT 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 G-phospholipase Cβ-protein kinase C (PKCε) pathway mediated by 5-HT 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 B (IB)-negative neurons; signals were inhibited by a 5-HT antagonist and PKCε blocker. Thus, 5-HT mediates 5-HT-induced mechanical hyperalgesia by regulating TRPV1 function. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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