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目的研究左旋多巴对帕金森病大鼠脑内多巴胺转运体的影响,探讨左旋多巴诱发异动症的可能机制。方法建立右侧毁损帕金森病大鼠模型,采用左旋多巴(20mg.kg-1.d-1)治疗1个月,停药2d后断头取脑,处死前3h尾静脉注射131I-FP-β-CIT,纹状体部位冠状振动切片,磷屏显影。图像分析系统分析每个切片中左、右纹状体区单位面积的特异性放射性摄取,用比值R左/右来评估多巴胺转运体的数量及功能。结果 (1)假手术组大鼠左右两侧右纹状体区多巴胺转运体对131I-FP-β-CIT特异性放射性摄取差异无统计学意义(左侧为419.407±14.267,右侧为437.604±19.046,P>0.05),R左/右=0.96±0.044;图像清晰,对称分布于基底节纹状体区。(2)帕金森病模型鼠损伤侧(右侧脑)放射性摄取明显减少(右侧284.052±105.84,P<0.01),R左/右值升高(R左/右=1.495±0.25,P<0.01),图像明显稀疏;(3)左旋多巴治疗组部分鼠损伤侧(右侧脑)放射性摄取进一步减少(右侧221.799±75.346,P<0.01),R左/右值较帕金森病模型组进一步升高(R左/右=2.06±0.60,P<0.05);图像中右侧基底节纹状体区更加稀疏,临床观察评分有异动症发生(53%)。结论经左旋多巴治疗后部分帕金森病鼠脑内多巴胺转运体的数目及功能进一步下调,对多巴胺能神经元有毒性作用,易促发异动症。
Objective To investigate the effect of levodopa on dopamine transporter in rat brain and to explore the possible mechanism of levodopa-induced dyskinesia. Methods The right rat lesioned Parkinson’s disease model was established and treated with levodopa (20 mg.kg-1.d-1) for 1 month. The brain was decapitated 2 days after drug withdrawal. The tail vein of 131I-FP -β-CIT, coronal striatum coronal section, phosphor screen. The image analysis system analyzes the specific radioactivity uptake per unit area of the left and right striatum regions in each slice and the ratio and R left / right to assess the number and function of the dopamine transporter. Results (1) There was no significant difference in the specific radioactive uptake of 131I-FP-β-CIT between right and left striatum in the sham operation group (419.407 ± 14.267 on the left and 437.604 ± on the right) 19.046, P> 0.05), R left / right = 0.96 ± 0.044; the image was clear and symmetrical in basal ganglia area. (2) The radioactive uptake of injured right (right) brain in Parkinson’s disease rats was significantly reduced (right 284.052 ± 105.84, P <0.01), R left / right increased (R left / right = 1.495 ± 0.25, P < 0.01), and the images were obviously sparse. (3) The radioactivity uptake of right and left brains of rats in the levodopa treatment group was further decreased (right side 221.799 ± 75.346, P <0.01) Group (R left / right = 2.06 ± 0.60, P <0.05); the right basal ganglion was more sparse in the image, and the clinical observation score had dyskinesia (53%). Conclusion The number and function of dopamine transporter in brain of some Parkinson’s disease rats after levodopa therapy are further downregulated, which have toxic effects on dopaminergic neurons and are easy to trigger dyskinesias.