當我們受傷時，身體的周邊組織會釋放出發炎調節因子使得傷害性接受器被活化和敏感，造成發炎性疼痛的產生。血清素是一種重要的發炎調節因子，會被周邊組織的血小板和肥大細胞所釋放出來，參與在疼痛以及痛覺敏感現象。先前研究發現血清素受體2B/2C抑制劑，會抑制由血清素所引發的機械性痛覺敏感現象，但並不能抑制熱痛覺敏感現象。然而，目前依然不清楚是透過何種訊號傳遞路徑來調控血清素引發的機械性痛覺敏感現象，以及哪一個血清素受體調控熱痛覺敏感現象。在我的實驗結果發現，血清素受體2B是透過磷脂酶Cβ-蛋白質激酶Cε路徑，調控血清素引發的機械性痛覺敏感現象，並且辣椒素受體1也參與在其中調控。血清素受體2B參與完全弗氏佐劑所引發的機械性痛覺敏感現象前期。血清素所引發的熱痛覺敏感現象，是由血清素受體2A透過磷脂酶Cβ-蛋白質激酶Cε路徑所調控的。;Following tissue damage, peripheral tissues release inflammatory mediators that activate and sensitize the nociceptors, inducing inflammatory pain. Serotonin (5-HT), one of the important inflammatory mediators, is released from platelets and mast cells and involved in pain and hyperalgesia. Previous studies have found that 5-HT2B/2C antagonist inhibits 5-HT-induced mechanical but not thermal hyperalgesia. However, it remains unclear which signaling pathways are involved in 5-HT-induced mechanical hyperalgesia and which 5-HT receptor mediates thermal hyperalgesia. I have found that 5-HT2B mediated 5-HT-induced mechanical hyperalgesia through phospholipase Cβ (PLCβ)-protein kinase Cε (PKCε) pathway. It was likely due to regulation of TRPV1. 5-HT2B is involved in CFA-induced mechanical hyperalgesia in the early phase. 5-HT-induced thermal hyperalgesia was mediated by 5-HT2A-Gq-PKCε pathway.
