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 dopamine D2 antagonist) respectively. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to measure the expression of NGFI-B mRNA in striatum and the behavior changes were observed. Results: 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.
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Xuebing Cao, Yixuan Niu, Yan Xu, Guanglei Yuan, Guirong Wei, Shenggang Sun. The role of nerve growth factor inducible protein B in the pathogenesis of levodopa-induced dyskinesias[J].,2006,20(2).