血清素 (Serotonin)是發炎物質的一種，並且主要表現在中樞和週邊神經系統。在受傷或是發炎後，血清素會從血小板或是肥大細胞釋放到週邊神經系統，並引起痛覺或是痛覺過敏。血清素受體共有七個亞型。然而目前還不清楚哪一個血清素受體和血清素引起的痛和痛覺過敏相關。在這篇論文裡，我研究血清素受體2B在血清素引起的痛和痛覺過敏中所扮演的角色。我發現注射血清素或是血清素2的促進劑會產生對機械性刺激的痛覺過敏。而血清素引起的機械性痛覺過敏可以被血清素受體2B/2C的抑制劑給抑制，但血清素受體2A的抑制劑不能抑制血清素引起的痛覺過敏，意指血清素受體2B或2C參與了血清素引起痛覺過敏。考慮到血清素受體2C沒有表現在背根神經節中，血清素受體2B參與血清素引起的機械性痛覺過敏中。進一步我想了解血清素受體2B調控機械性痛覺過敏的機制，我共同轉染了血清素受體2B和與痛覺過敏相關的離子通道(例如酸敏感離子通道家族或辣椒素受體1)到人類胚胎腎臟細胞中，並且以鈣離子攝影驗證血清素受體2B是否會調控這些離子通道。 Serotonin (5-hydroxtryptamine [5-HT]) is one of the inflammatory mediators present in central and peripheral nervous system. After injury or inflammation, 5-HT is released from platelets and mast cells to peripheral nervous system, causing pain and hyperalgesia. 5-HT receptors include seven subtypes (5HT1-7). However, it remains unclear which subtype of 5-HT receptors is involved in 5-HT-induced pain and hyperalgesia. In this study, we have investigated the roles of 5-HT2B receptors in 5-HT-induced pain and hyperalgesia. We have found that injection of 5-HT or 5-HT2 agonist ?-m-5HT produces significant hyperalgesia to mechanical stimuli. The mechanical hyperalgesia induced by 5-HT injection is inhibited by 5-HT2B/2C antagonist SB206553, but not 5-HT2A antagonist Ketanserin, suggesting that 5-HT2B or 5-HT2C receptors are involved in 5-HT-induced mechanical hyperalgesia. Given that 5-HT2C receptor is not present in not present in DRG, it could be 5-HT2B receptor involved in 5-HT-induced mechanical hyperalgesia. To further understand the mechanism of 5HT2B-mediated mechanical hyperalgesia, we co-transfect 5-HT2B and ion channels that are related to hyperalgesia (such as ASICs or TRPV1) to human embryo kidney 293T cells (HEK293T), and examine whether 5-HT2B receptor regulates these ion channels by calcium image.
