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目的探讨纹状体神经元电生理活动的变化在左旋多巴诱发异动症(LID)发生中的作用及意义。方法32只大鼠共分为3组：对照组(n=10),帕金森病(PD)组(n=12),LID组(n=10)。6-羟基多巴胺(6-OHDA)立体定位注射制备偏侧PD大鼠模型,左旋多巴腹腔注射治疗4周诱发LID大鼠模型。两组模型分别尾静脉注射多巴胺D1、D2受体激动剂SKF-38393、quinpirole,受体拮抗剂SCH-23390、haloperidol,采用微电极细胞外记录技术检测纹状体棘状神经元(SMSNs)电生理活动的变化。结果LID组SMSNs的自发性电活动较对照组及PD组明显增多(P＜0．05)。SKF-38393对LID组SMSNs自发性电活动的抑制作用呈浓度依赖性,LID组SMSNs的半抑制浓度(IC50)较PD组明显下降(P＜0．05)。Quinpirole对LID组SMSNs的IC50与PD组相比无显著性差异(P＞0．05)。结论LID大鼠SMSNs的自发性电活动增强,D1受体介导的神经元电活动敏感性增高。
Objective To investigate the role and significance of changes in electrophysiological activity of striatal neurons in the development of levodopa-induced dyskinesia (LID). Methods Thirty - two rats were divided into three groups: control group (n = 10), PD group (n = 12) and LID group (n = 10). L-dopamine (6-OHDA) stereotactic injection of hemizygous PD rat model, L-dopa intraperitoneal injection for 4 weeks induced LID rat model. The dopaminergic D1 and D2 receptor agonists SKF-38393, quinpirole, and receptor antagonist SCH-23390 and haloperidol were injected into the caudal vein of rats in each group via tail vein. Microelectrode extracellular recording technique was used to detect the number of rat spinous neurons (SMSNs) Changes in physical activity. Results The spontaneous electrical activity of SMSNs in LID group was significantly higher than that in control group and PD group (P <0.05). The inhibitory effect of SKF-38393 on spontaneous electrical activity of SMSNs in LID group was concentration-dependent, and the half-inhibitory concentration (IC50) of SMSNs in LID group was significantly lower than that of PD group (P <0.05). The IC50 of Quinpirole to SMSNs in LID group was not significantly different from that in PD group (P> 0.05). Conclusion The spontaneous electrical activity of SMSNs is increased in LID rats, and the sensitivities of D1 receptor-mediated neuronal electrical activity increase.