The Regulation Of High Expressional Transcription Factorâ–³ FosB On NMDAR1 In The Striaturn Of Dyskinesia Rat

objective To study the role ofΔFosB high expression in striatum in the development of levodopa-induced-dyskinesia(LID) and the influence on the pathway of glutamate receptors.Methods The hemiparkinsonian rat model was established by 6-hydroxydopamine (6-OHDA) injection stereotaxically.Then the models were divided into two groups: experimental group and control group.The rats in experimental group were used to inject rAAV2-ΔFosB-EGFP stereotaxically, and the rAAV-EGFP was injected into the rats in control group instead.Both of the groups were also divided into four subgroups,the rats in subgroups were kept seperately for 3 weeks,6 weeks,9 weeks and 12 weeks.Then all the rats accept single injection of levodopa, and the AIM scores were evaluated. The expression of FosB/ΔFosB in the striatum was detected by inmunohistochemistry, the changes ofΔFosB, NMDAR1 total protein and NMDAR1 ser896 phosphorylated protein were checked by western blot.Results dyskinesia can not be seen obviously in the rats in control subgroups , All the rats in experimental subgroups showed typical dyskinesia,the AIM scores of 3w,6w,9w and 12w experimental subgroups are separately 22.89±2.53;37.38±4.96;47.38±4.14;50.25±5.23, and as time increased,the AIM scores were increased gradually. The level ofΔFosB in the rats in experimental group were much higher than that in control group. The levels of NMDAR1 protein and NMDAR1 ser896 phosphorylated protein in experimental group were aslo higher than that in control group.Conclusion The striatal high expression ofΔFosB in PD rats were related closely to the development of dyskinesia. The level ofΔFosB was positively correlated to the AIM scores.We can established parkinsonian rat model by injecting rAAV-ΔFosB into the striatum of rats andΔFosB may involve the development of dyskinesia by mediating the expression of NMDAR1 and phosphorylated protein.