The druggable approach using small nucleolar RNA of the neuropathic pain

5 -羟色胺2C受体（5HTR2C）接受RNA编辑。众所周知，由于5HTR2C的选择性剪接，会发生火焰转移，并产生非功能性受体。研究了5HTR2C RNA编辑在大鼠口腔-面部神经性疼痛模型中的效率（Nakae et al.）。EJN 2008)，我们的兴趣转向了有助于RNA编辑的因素和选择性剪接的有效性。在人体研究中，HBII-52（一种与RBII-52功能相同的核小RNA）参与调控5HTR2C RNA的编辑和选择性剪接。本研究采用眶下松结扎模型。RBII-52在损伤和假手术动物中的表达趋势降低。另一方面，损伤大鼠和假手术大鼠只有含有Va的模式（非功能性）增加。RBII-52表达、5HT2C-R选择性剪接和RNA编辑之间的关系尚不清楚。5HTR2C活动的调节可能比我们之前想象的通过有害刺激反应（如神经性疼痛）进行的调节要精细得多。

The serotonin 2C receptor (5HTR2C) receives RNA editing. It is also known that as a result of alternative splicing of the 5HTR2C, a flame shift occurs and a non-functional receptor is created. Having studied the 5HTR2C RNA editing efficiency in a rat oro-facial neuropathic pain model (Nakae et al. EJN 2008), our interest turned to the factor contributing to RNA editing and efficacy of alternative splicing. In human study, HBII-52 (one kind of small nuclear RNA ; equal in function to RBII-52) contributes to regulating the 5HTR2C RNA editing and alternative splicing. In this research, an infra-orbital loose ligation model was used. The tendency of RBII-52 expression in injured and sham operated animals decreased. On the other hand, only the Va containing pattern (non-functional) increased in injured and sham rats. The relationship between RBII-52 expression, the 5HT2C-R alternative splicing and RNA editing was unclear. Modulation of 5HTR2C activity might be capable of far finer tuning than we previously imagined through noxious stimuli response, such as neuropathic pain.