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Mechanism of over-activation in direct pathway mediated by dopamine D_1 receptor in rats with levodopa-induced dyskinesias

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Neuroscience Bulletin 2006年第3期22卷 159-164页

作者： Xue-Bing CAO Qiang GUAN Yan XU Lan WANG Sheng-Gang SUN Department of Neurology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China

Objective To study the changes of prodynorphin （PDyn） gene expression and dopamine and cAMPregulated phosphoprotein of 32 kDa （DARPP-32） phosphorylation in rats with levodopa-induced dyskinesias （LID）, and to explore the mechanism of over-activation in direct pathway mediated by dopamine D1 receptor. Methods Parkinson＇s disease （PD） rats were received levodopa （10 mg/kg, i.p.） for 28 d to get the LID rats. According to the behavior scale, LID rats were divided into mild （n=8） and severe （n=16） groups. On day 29, 8 rats in severe LID group were given an acute intraperitoneal injection of MK-801 （0.1 mg/kg） 15 min before levodopa treatment （MK-801 group, n=8）. The normal rats received same course and dosage of levodopa as the control group （n=8）. Hybridization in situ was used to measure the expression of PDyn mRNA in striatum. Protein and mRNA levels of total DARPP-32 and phospho-Thr-34 DARPP-32 level were measured by immunoblotting and RT-PCR, respectively. Results The levels of PDyn mRNA and phospho-Thr-34 DARPP-32 increased significantly in LID rats compared with control rats （P〈0.01）, and they also increased markedly in severe LID group compared with mild group （P〈0.01）. Conclusion Phospho-Thr-34 DARPP-32 level was increased in LID rats, which contributed to the over-activation of direct pathway mediated by dopamine D1 receptor.

关键词： levodopa-induced dyskinesias Prodynorphin Dopamine and cAMP-regulated phosphoprotein of 32 kDa

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The role of nerve growth factor inducible protein B in the pathogenesis of levodopa-induced dyskinesias

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Journal of Nanjing Medical University 2006年第2期20卷 79-82页

作者： Xuebing Cao Yixuan Niu Yan Xu Guanglei Yuan Guirong Wei Shenggang Sun Department of Neurology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022China

Objective： To study the role of the expression of nerve growth factor inducible protein B gene （NGFI-B） in striatum in the pathogenesis of levodopa-induced dyskinesias （LID）. Methods： The rat model of LID was treated with SCH 23390（1 mg/kg ip,a dopamine D1 antagonist） and haloperidol （1 mg/kg ip,a dopanfme D2 antagonist） respectively. Reverse transcriptase-polymerase chain reaction （RT-PCR） was used to measure the expression of NGFI-B mRNA in stiiatam and the behavior changes were observed. Resuits： After treatment with SCH23390, abnormal involuntary movement （AIM） in LID rats was decreased （ P 〈 0.05 ） and the expression of NGFI-B mRNA in striatum did not change significantly. After treatment with haloperidol, the changes of AIM in LID rats were not significant and the expression of NGFI-B mRNA was increased significantly（ P 〈 0.01）. Conclusion： LID is associated with over-expression of NGFI-B in striatum. Abnormal activity in the direct pathway and the basal ganglia circuit could be involved in the occurrence of LID.

关键词： levodopa-induced dyskinesias levodopa Parkinson' s disease nerve growth factor inducible proteinB

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