慢性神经病理性疼痛引起的焦虑、抑郁等负性情绪严重影响患者的生活及预后，杏仁核内部环路异常可能与之密切相关，但具体的中枢机制仍不甚明了。SLITRK1是一种存在于神经系统、具有调节突触可塑性作用的跨膜蛋白，其基因缺陷小鼠出现焦虑或抑郁样行为。我们的前期研究发现:慢性神经病理性疼痛小鼠脑中基底外侧杏仁核（BLA）的SLITRK1表达随疼痛阈值的降低呈递减趋势；敲减正常小鼠BLA的SLITRK1后，焦虑、抑郁倾向明显增加,提示SLITRK1可能通过调节该脑区的突触可塑性参与慢性神经病理性疼痛负性情绪的病理机制。课题组拟进一步应用分子学、行为学和电生理技术明确SLITRK1与慢性神经病理性疼痛负性情绪的关系、研究SLITRK1对杏仁核内部环路突触可塑性的影响并探索过表达小鼠杏仁核中SLITRK1是否可以逆转慢性神经病理性疼痛负性情绪，揭示慢性神经病理性疼痛继发焦虑、抑郁等负性情绪的细胞与分子机制。

Negative emotions like anxiety and depression induced by chronic neuropathic pain seriously impair life and prognosis of the patients. The abnormal internal loop of amygdala may be involved in it but the specific mechanism is still unclear. SLITRK1 is a transmembrane protein that exists in the central nervous system and regulates synaptic plasticity. SLITRK1-deficient mice showed anxiety/depression-like behavior. We previously found that the expression of SLITRK1 in basolateral amygdala (BLA) of mice with chronic neuropathic pain decreased by the downward trend of pain threshold. Besides, wild type mice obviously showed anxiety/depression-like behavior after conditional knockdown of SLITRK1 in BLA. These results suggest that SLITRK1 may be involved in the pathological mechanism of negative emotions secondary to chronic neuropathic pain by regulating synaptic plasticity. We intend to further clarify the relationship between SLITRK1 and negative emotions induced by chronic neuropathic pain and study the effect of SLITRK1 on synaptic plasticity in the internal loop of amygdala by molecular, behavioral and electrophysiological techniques. Over expression of SLITRK1 in amygdala will be conducted to explore whether it can reverse the negative emotions secondary to chronic neuropathic pain. The purpose of this study was to reveal the cellular and molecular mechanisms of negative emotions such as anxiety and depression induced by chronic neuropathic pain.