CAJ | 학술논문

目的评价神经病理性痛大鼠内侧额叶前皮质γ-氨基丁酸Aα1亚型(GABAAα1)受体表达的变化.方法成年雄性Wistar大鼠9只,体重200～210 g,采用随机数字表法,将其随机分为3组(n=3):对照组(C组)、假手术组(s组)和神经病理性痛组(P组).P组采用坐骨神经慢性压迫法制备大鼠神经病理性痛模型;S组只暴露坐骨神经,而不结扎.于术前1 d和术后1、4、7、10、14 d时,测定机械痛阈和热痛阈.痛阈测定结束后,处死大鼠,取内侧额叶前皮质,采用Western blot法检测GABAAα1受体的表达.结果与C组和S组比较,P组术后各时点机械痛阈和热痛阈降低,内侧额叶前皮质GABAAα1受体表达上调(P＜0.01);C组和S组间机械痛阈、热痛阈和内侧额叶前皮质GABAAα1受体表达比较差异无统计学意义(P＞0.05).结论内侧额叶前皮质GABAAα1受体表达上调可能参与了大鼠神经病理性痛的形成与维持.
목적 평개신경병이성통대서내측액협전피질γ-안기정산Aα1아형(GABAAα1)수체표체적변화.방법 성년웅성Wistar대서9지,체중200～210 g,채용수궤수자표법,장기수궤분위3조(n=3):대조조(C조)、가수술조(s조)화신경병이성통조(P조).P조채용좌골신경만성압박법제비대서신경병이성통모형;S조지폭로좌골신경,이불결찰.우술전1 d화술후1、4、7、10、14 d시,측정궤계통역화열통역.통역측정결속후,처사대서,취내측액협전피질,채용Western blot법검측GABAAα1수체적표체.결과 여C조화S조비교,P조술후각시점궤계통역화열통역강저,내측액협전피질GABAAα1수체표체상조(P＜0.01);C조화S조간궤계통역、열통역화내측액협전피질GABAAα1수체표체비교차이무통계학의의(P＞0.05).결론 내측액협전피질GABAAα1수체표체상조가능삼여료대서신경병이성통적형성여유지.
Objective To investigate the changes in the expression of GABAAα1, receptors in medial prefrontal cortex (mPFC) in a rat model of neuropathic pain. Methods Nine male Wistar rats weighing 200-210 g were randomly divided into 3 groups ( n = 3 each): control group (group C) , sham operation group (group S) and neuropathic pain group (group P). Neuropathic pain was induced by chronic constrictive injury. The right sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 3-0 chromic catgut. In group S, the right sciatic nerve was exposed but not ligated. The thermal and mechanical pain threshold was measured at 1 d before and 1,4,7, 10 and 14 d after operation. The animals were then sacrificed and the mPFC was removed. The expression of GABAAα1, receptors in mPFC was determined by Western blot. Results Compared with C and S groups, thermal and mechanical pain threshold were significantly decreased and the expression of GABAAα1, receptors was up-regulated in group P ( P ＜ 0.01) . There was no significant difference was in the thermal and mechanical pain threshold and expression of GABAAα1 receptors between C and S groups (P ＞ 0.05). Conclusion Up-regulation of GABAAα1 receptor expression in mPFC may be involved in the development and maintenance of neuropathic pain in rats.