The druggable approach using small nucleolar RNA of the neuropathic pain

5-羟色胺2C受体（5 HTR 2C）接受RNA编辑。还已知，由于5 HTR 2C的选择性剪接，发生火焰转移并产生非功能性受体。在大鼠口面神经性疼痛模型中研究了5 HTR 2C RNA编辑效率（Nakae et al. EJN 2008）后，我们的兴趣转向了有助于RNA编辑的因素和选择性剪接的功效。在人体研究中，HBII-52（一种核内小RNA，功能与RBII-52相当）参与调节5 HTR 2C RNA编辑和选择性剪接。在本研究中，使用眶下松结扎模型。损伤组和假手术组RBII-52表达呈下降趋势。另一方面，只有Va包含模式（非功能性）在受伤和假手术大鼠增加。RBII-52表达、5 HT 2C-R选择性剪接和RNA编辑之间的关系尚不清楚。5 HTR 2C活性的调节可能比我们以前想象的更精细，通过伤害性刺激反应，如神经性疼痛。

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.