Dopaminergic regulation of AP-1 transcription factor DNA binding activity in rat striatum

被引:18
|
作者
Huang, KX [1 ]
Walters, JR [1 ]
机构
[1] NINCDS, EXPT THERAPEUT BRANCH, NATL INST HLTH, BETHESDA, MD 20892 USA
关键词
6-hydroxydopamine; reserpine; nigrostriatal; SKF; 38393; Parkinsonism; immediate early gene;
D O I
10.1016/0306-4522(96)00229-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Dopaminergic modulation of the DNA binding activity of AP-1, Sp1, CREB and AP-2 transcription factors was examined in rat striatal nuclear extracts by gel shift assay. AP-1 binding was selectively increased in the striatum following depletion of dopamine by 6-hydroxydopamine-induced lesion of the nigrostriatal pathway or after reserpine treatment. The D-1 agonist SKF 38393 dose-dependently increased AP-1 binding; this effect was significantly increased in reserpine-treated rats and even more markedly enhanced in denervated striatum. The D-2/D-3 agonist quinpirole, administered alone, did not affect striatal activator protein-1 binding; in combination, quinpirole and SKF 38393 acted synergistically in normal and reserpine-treated rats but not in 6-hydroxydopamine-lesioned rats, suggesting that mechanisms underlying D-1-D-2/D-3 interactions are altered after dopamine denervation. Most, but not all, of the changes in AP-1 binding activity observed in this study are consistent with changes in levels of Fos/Jun family proteins observed after similar treatments. These results support the hypothesis that D-1 receptor stimulation activates striatonigral neurons and modulates expression of AP-1-related genes in these neurons, while D-2 receptor stimulation mediates tonic inhibition of AP-1 expression and activity in the striatopallidal neurons. Moreover, the findings provide evidence that the loss of dopaminergic input to the striatum, as occurs in Parkinson's disease, induces long-lasting alterations in the regulation of striatal gene expression which may contribute to the disease's progress.
引用
收藏
页码:757 / 775
页数:19
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