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为了研究皮层电刺激对左旋多巴诱发异动症(LID)大鼠纹状体神经元c-fos及脑啡肽(ENK)表达的影响,探讨皮层-纹状体通路可塑性改变在LID发生机制中的作用,本实验制备Parkinson病(PD)和LID大鼠模型,将实验大鼠分成三组:正常对照组、PD组和LID组。电刺激运动皮层后,免疫组化法检测纹状体区c-fos、ENK、细胞外信号调节激酶1/2(ERK1/2)及其活化形式磷酸化细胞外信号调节激酶1/2(p-ERK1/2)的表达。结果显示:与对侧比较,皮层电刺激使各组同侧纹状体c-fos、ENK、ERK1/2、p-ERK1/2表达均增加(P<0.01);LID组c-fos(0.67±0.03)以及p-ERK1/2的表达(0.17±0.05)较PD组(0.08±0.03)和正常组(0.07±0.02)增加(P<0.05),LID组ENK(0.21±0.07)的表达和PD组(0.18±0.08)相比较无统计学差异(P>0.05),但均较正常组(0.08±0.01)增加(P<0.01);三组ERK1/2的表达无统计学差异(P>0.05),但LID组p-ERK1/2的表达(0.17±0.05)较PD组和正常组有所增加(P<0.01)。本研究结果表明,LID大鼠皮层-纹状体通路兴奋使纹状体c-fos以及p-ERK1/2表达增加,ENK的表达没有显著变化。上述结果提示皮层-纹状体通路活动增强以及p-ERK1/2表达的增加与LID的发生机制有关,而ENK在LID的发生过程中可能不发挥重要作用。
To investigate the effect of cortical stimulation on the expression of c-fos and enkephalin (ENK) in striatum neurons of LID rats and to explore the role of cortical-striatal pathway plasticity in the pathogenesis of LID In this experiment, Parkinson’s disease (PD) and LID rat model were prepared. The experimental rats were divided into three groups: normal control group, PD group and LID group. After electrical stimulation of the motor cortex, expressions of c-fos, ENK, extracellular signal-regulated kinase 1/2 (ERK1 / 2) and its activated form of phosphorylated extracellular signal-regulated kinase 1/2 -ERK1 / 2) expression. The results showed that the expression of c-fos, ENK, ERK1 / 2 and p-ERK1 / 2 were increased in the ipsilateral striatum compared with the contralateral ones (P <0.01) (P <0.05). The expression of ENK (0.21 ± 0.07) in LID group was significantly higher than that in PD group (0.08 ± 0.03) and normal group (0.07 ± 0.02) PD group (0.18 ± 0.08) (P> 0.05), but both of them were significantly higher than those in normal group (0.08 ± 0.01) (P <0.01). There was no significant difference in ERK1 / 2 expression among three groups (P> 0.05). However, the expression of p-ERK1 / 2 in LID group (0.17 ± 0.05) was higher than that in PD group and normal group (P <0.01). The results of this study show that the excitatory cortical-striatal pathway in LID rats increased the expression of c-fos and p-ERK1 / 2 in striatum, while the expression of ENK did not change significantly. The above results suggest that increased cortical-striatal pathway activity and increased expression of p-ERK1 / 2 are associated with the pathogenesis of LID, whereas ENK may not play an important role in the development of LID.