瑞芬太尼引发痛觉过敏临床常见，尚无可靠治疗方法。最新研究显示TMEM16C/Slack通路具有调节痛觉信息传递作用。我们已发表的成果证实含有GluR1亚基AMPA受体表达和功能增加在促进瑞芬太尼痛觉过敏中扮演着重要角色，但含GluR1亚基AMPA受体通过那个通路引起相关作用尚未阐述。本项目将利用切口痛-瑞芬太尼痛觉过敏模型，从在体实验和离体背根神经节培养两个水平，应用热板、Von Frey test、Western Blot、免疫荧光、免疫共沉淀以及膜片钳技术对TMEM16C、Slack以及AMPAR受体GluR1亚基在瑞芬太尼痛觉过敏中的表达和功能的动态变化进行研究，并利用TMEM16C基因沉默和过表达技术，以及含GluR1亚基AMPA受体抑制剂PhTX探讨TMEM16C/Slack—GluR1通路在瑞芬太尼诱发痛觉过敏中的调控机制。本研究将为瑞芬太尼痛觉过敏现象的临床防治提供新思路。

The incidence of remifentanil-induced hyperalgesia is much higher than other opioids. Until now, there is no effective solution to prevent this phenomenon. The recent studies suggest that TMEM16C/Slack signaling plays a pivotal role in the modulation of pain transmission. Our previous studies suggest that GluR1-containing AMPA receptor plays an important role in remifentanil-induced hyperalgesia via modulate AMPA receptor GluR1 subunit trafficking and receptor function. However, which signaling modulate this phenomenon has not reported yet. This program will use a rat model with incision pain-remifentani-induced hyperalgesia to detect the role of TMEM16C/Slack-CluR1 signaling in remifentanil-induced hyperalgesia. In this study, we use Hot plate test, Von Frey test, Western Blot, Immunofluorescence, Co-IP and Patch-clamp recording to detect the expression and function changes of TMEM16C, Slack and AMPA receptor GluR1 subunit in remifentanil-induced hyperalgesia rats. We also use TMEM16C knockdown and overexpression and GluR1 containing AMPA receptor inhibitor PhTX to demonstrate the role of TMEM16C/Slack—GluR1 signaling in remifentanil-induced hyperalgesia. The current study will provide a new idea for effective prevention and treatment of remifentanil-induced hyperalgesia.