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作 者:解新[1] 蔡捷[1] 万有[1] 崔彦军[2] 邢国刚[1]
机构地区:[1]北京大学神经科学研究所基础医学院神经生物学系,教育部和卫生部神经科学重点实验室,北京100191 [2]北京大学医院内科,北京100871
出 处:《中国疼痛医学杂志》2014年第9期616-619,共4页Chinese Journal of Pain Medicine
基 金:国家自然科学基金(81371237;31171063);科技部国家重点基础研究发展计划"973"资助项目(2013CB5131905);卫生部行业专项基金(20130293-01);北京市自然科学基金(7112079)资助
摘 要:目的:研究脊神经结扎(SNL)后大鼠脊髓背角SFKs-Y416p和GluN2B的表达变化,并探讨二者在维持神经病理性疼痛中的作用。方法:按照双盲随机的原则,将20只雄性SD大鼠随机分为Naive组(n=4),SNL手术组(n=8)和假手术组(n=8),进行Western blotting实验,检测神经病理性疼痛大鼠脊髓背角突触部位SFKs-Y416p和GluN2B的表达变化。结果:1 Western blotting定量分析显示,脊神经结扎能显著上调SFKs-Y416p。SNL后第7 d,脊髓背角突触部位的SFKs-Y416p由手术前的(0.89±0.07)上调到(1.27±0.08)(P<0.01);然而在假手术组大鼠,背角突触部位的SFKs-Y416p则没有明显的变化。2 SNL后第7 d,脊髓背角突触部位的GluN2B由术前的(0.73±0.05)上调到(1.45±0.12)(P<0.01);然而在假手术组大鼠,背角突触部位的GluN2B则没有明显变化。结论:脊神经结扎可以上调脊髓背角突触部位SFKs-Y416p和GluN2B的蛋白表达,且SFKs-Y416p和GluN2B升高的时间点在神经病理性疼痛的第7天,所以,SFKs-Y416p/GluN2B信号通路可能参与维持外周神经损伤所引起的神经病理性疼痛的中枢机制。Objective: To investigate the changes of SFKs-Y416p and GluN2B content in the spinal dorsal horn in spinal nerve ligated (SNL) rats and to explore the role of spinal SFKs-Y416p and GluN2B in the maintenance of neuropathic pain. Methods: Twenty male Sprague-Dawley rats were randomly divided into Naive group (n = 4), SNL-operated group (n = 8), and sham-operated group (n = 8). The changes of SFKs- Y416p and GluN2B in the spinal dorsal horn of SNL- or sham-operated rats were detected by Western blotting techniques. Results:0) The SFKs-Y416p content in the synapse measured by Western blotting was significantly increased after spinal nerve ligation. At seven days after surgery in SNL rats, SFKs-Y416p content in the synaptic area increased to ( 1.27±0.08 ) from ( 0.89±0.07 ) ofpre-operation (P 〈 0.01). No significant changes in the SFKs-Y416p content were observed in sham rats. (2) At seven days after surgery in SNL rats, the GIuN2B content in the synaptic area was also increased significantly. The GluN2B content in the synaptic area increased to ( 1.45±0.12 ) from ( 0.73±0.05 ) of pre-operation (P 〈 0.01). No significant changes in the GluN2B content was observed in sham rats. Conclusion: Up-regulation of the synaptic SFKs-Y416p andGIuN2B content in the spinal dorsal horn occurred in SNL rats. Moreover, the increasing time of SFKs-Y416p and GluN2B is at seven days after spinal nerve ligation. Therefore, the SFKs-Y416p/GluN2B signaling plays an important role in the maintenance of neuropathic pain at the late stage of nerve injury.
关 键 词:SFKs-Y416p GluN2B 脊髓背角 神经病理性疼痛 突触小体 脊神经结扎 大鼠
分 类 号:R744[医药卫生—神经病学与精神病学]
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