CAJ | 학술논문

目的:研究δ-阿片受体表达和激活对钠通道1.2亚型的电流特性的影响.方法:用双电极电压钳技术,在δ-阿片受体和钠通道亚型1.2共表达的非洲爪蟾第V期卵母细胞上,观察δ-阿片受体表达和/或激活后,钠通道1.2亚型电流特性的变化.结果:1)钠通道1.2亚型的表达产生河豚毒素(tetrodotoxin,TTX)敏感的内向电流;2)δ-阿片受体的表达减少钠通道激活电流的幅度;3)δ-阿片受体和钠通道1.2亚型共表达的卵母细胞中,δ-阿片受体激动剂可以抑制钠通道激活电流的幅度和电导,而只有钠通道1.2亚型表达的卵母细胞则无此现象;4)δ-阿片受体激动剂抑制钠电流的作用具有剂量依赖关系,并能达到饱和状态;5)δ-阿片受体激动剂对未表达外派陛蛋白的卵母细胞无影响.结论:本结果首次以直接证据证明了δ-阿片受体可以抑制钠通道的兴奋性和降低钠电流的幅度.这一发现对缺血/缺氧性神经元损伤、癫痫、疼痛等神经机能障碍的解决具有深远意义,并有助于深入揭示针刺治疗脑疾病的内在机制.
목적:연구δ-아편수체표체화격활대납통도1.2아형적전류특성적영향.방법:용쌍전겁전압겸기술,재δ-아편수체화납통도아형1.2공표체적비주조섬제V기란모세포상,관찰δ-아편수체표체화/혹격활후,납통도1.2아형전류특성적변화.결과:1)납통도1.2아형적표체산생하돈독소(tetrodotoxin,TTX)민감적내향전류;2)δ-아편수체적표체감소납통도격활전류적폭도;3)δ-아편수체화납통도1.2아형공표체적란모세포중,δ-아편수체격동제가이억제납통도격활전류적폭도화전도,이지유납통도1.2아형표체적란모세포칙무차현상;4)δ-아편수체격동제억제납전류적작용구유제량의뢰관계,병능체도포화상태;5)δ-아편수체격동제대미표체외파폐단백적란모세포무영향.결론:본결과수차이직접증거증명료δ-아편수체가이억제납통도적흥강성화강저납전류적폭도.저일발현대결혈/결양성신경원손상、전간、동통등신경궤능장애적해결구유심원의의,병유조우심입게시침자치료뇌질병적내재궤제.
Objective: To study the precise role of DOR in the regulation of sodium channels at present. Methods: With Xenopus oocytes co-expressing sodium channel subtype 2 (Nav1.2) and DOR. Results: 1) Nav1.2 expression induced tetrodotoxin-sensitive inward currents; 2) DOR expression reduced the inward currents; 3) activation of DOR reduced the amplitude of the current and rightly shifted the activation curve of the current in the oocytes with both Nav1.2 and DOR, but not in ones with Nav1.2 alone; 4) the DOR agonist-induced inhibition of Nav1.2 currents was in a dose-dependent manner and saturable; 5) the DOR agonist had no effect on naive oocytes. Conclusion: These data represent the first demonstration that activation of DOR inhibits Na+ channel function by decreasing the amplitude of sodium currents and increasing its threshold of activation. This novel finding has far-reaching impacts on novel solutions of certain neurological disorders such as hypoxic/ischemic injury, epilepsy and pain. Also, our data may improve the understanding of the mechanisms underlying acupuncture since acupuncture is known to activate the brain opioid system.