在mptp处理的小鼠菌株中,proenkephalin和prodynorphin基因的表达以及多巴胺能药物对c-fos基因的诱导均未发生改变。

B Ziolkowska, G Horn, A Kupsch, V Höllt
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引用次数: 7

摘要

研究了1-甲基-4-苯基-1,2,3,6,-四氢吡啶(MPTP)治疗后C57B1/6小鼠纹状体中proenkephalin (PENK)、prodynorphin (PDYN)和c-fos基因的表达。全身给药MPTP (2 × 40 mg/kg,间隔18小时)2周后,黑质(SN)损伤可见于黑质酪氨酸羟化酶(TH) mRNA杂交信号丢失,纹状体多巴胺水平下降91%。与未治疗的对照组相比,受损小鼠纹状体中PENK和PDYN mrna的水平没有显著变化。多巴胺D2受体拮抗剂氟哌啶醇对直接早期基因c-fos的诱导作用没有改变,而选择性D1受体激动剂SKF 38393未能在mptp处理的小鼠纹状体中诱导c-fos。这些结果与另一种PD啮齿动物模型大鼠的6-羟基多巴胺(6-OHDA)损伤的数据形成对比。在6- ohda损伤大鼠纹状体中,PENK基因上调,PDYN基因下调,D2受体拮抗剂对c-fos基因的诱导被取消,而选择性D1受体激动剂诱导的c-fos基因在非损伤大鼠中没有发生。我们推测,小鼠MPTP病变对纹状体基因表达影响不足主要是由于纹状体多巴胺消耗不足,在本模型中无法增加。在PD的小鼠和灵长类动物MPTP模型的背景下,已经讨论了6- ohda损伤大鼠中观察到的变化的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The expression of proenkephalin and prodynorphin genes and the induction of c-fos gene by dopaminergic drugs are not altered in the straitum of MPTP-treated mice.

The expression of proenkephalin (PENK), prodynorphin (PDYN) and c-fos genes was studied in the striatum of C57B1/6 mice treated with 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine (MPTP), which are used as a rodent model of Parkinson's disease (PD). Two weeks after systemic administration of MPTP (2 x 40 mg/kg, s.c. 18h apart), the lesion of the substantia nigra (SN) could be visualised by loss of the nigral tyrosine hydroxylase (TH) mRNA hybridization signal and by a 91% decrease in striatal dopamine levels. The levels of PENK and PDYN mRNAs were not significantly changed in the striatum of the lesioned mice, as compared to non-treated controls. The induction of the immediate early gene c-fos by the dopamine D2 receptor antagonist haloperidol was not altered, while the selective D1 receptor agonist SKF 38393 failed to induce c-fos in the striatum of MPTP-treated mice. These results are in contrast to the data concerning rats with the 6-hydroxydopamine (6-OHDA) lesion of the SN, which serve as another rodent model of PD. In the striata of 6-OHDA-lesioned rats, PENK gene is upregulated, PDYN gene is down-regulated and the induction of c-fos gene by D2 receptor antagonists is abolished, whereas selective D1 receptor agonists induce c-fos gene, which does not occur in non-lesioned rats. We presume that the lack of influence of the MPTP lesion in mice on the striatal gene expression was mainly caused by insufficient dopamine depletion in the striatum, which could not be increased in this model. The importance of the changes observed in 6-OHDA-lesioned rats has been discussed in the context of the mouse and primate MPTP models of PD.

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