Transfection of tyrosine kinase deleted FGF receptor-1 into rat brain substantia nigra reduces the number of tyrosine hydroxylase expressing neurons and decreases concentration levels of striatal dopamine

Molecular Brain Research Pub Date : 2005-10-03 DOI:10.1016/j.molbrainres.2005.05.032

Thomas D. Corso , German Torres , Christopher Goulah , Indrajit Roy , Angelo S. Gambino , John Nayda , Timothy Buckley , Ewa K. Stachowiak , Earl J. Bergey , Haridas Pudavar , Purnendu Dutta , David C. Bloom , William J. Bowers , Michal K. Stachowiak

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引用次数: 28

Abstract

The effects of HSV-1 amplicon and polyethyleneimine (PEI)-mediated transfection of dominant negative FGF receptor-1 mutant FGFR1(TK−) into the rat brain substantia nigra (SN) were examined in vivo to model the reduced FGF signaling documented to occur in Parkinson's disease. The number of SN neurons that expressed tyrosine hydroxylase (TH) was significantly reduced following HSV-1 FGFR1(TK−) intranigral delivery and similar changes were observed after PEI-mediated FGFR1(TK−) transfections. Further, we also observed a significantly lower striatal dopamine content following the PEI transfection of FGFR1(TK−). Thus, we conclude that reduced FGF signaling in the SN of Parkinsonian patients could play a role in the impaired dopaminergic transmission associated with the degenerative disease.

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将酪氨酸激酶缺失的FGF受体-1转染大鼠脑黑质，可减少表达酪氨酸羟化酶的神经元数量，降低纹状体多巴胺浓度水平

在体内研究了HSV-1扩增子和PEI介导的显性阴性FGF受体-1突变体FGFR1(TK -)转染大鼠脑黑质(SN)的作用，以模拟帕金森病中记录的FGF信号减少。表达酪氨酸羟化酶(TH)的SN神经元数量在HSV-1 FGFR1(TK -)内传递后显著减少，pei介导的FGFR1(TK -)转染后也观察到类似的变化。此外，我们还观察到PEI转染FGFR1(TK−)后纹状体多巴胺含量显著降低。因此，我们得出结论，帕金森患者SN中FGF信号的减少可能在与退行性疾病相关的多巴胺能传递受损中起作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Molecular Brain Research

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