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
{"title":"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","authors":"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","doi":"10.1016/j.molbrainres.2005.05.032","DOIUrl":null,"url":null,"abstract":"<div><p><span>The effects of HSV-1 amplicon and </span>polyethyleneimine<span><span> (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 </span>Parkinson's disease<span><span>. 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 </span>dopaminergic transmission associated with the degenerative disease.</span></span></p></div>","PeriodicalId":100932,"journal":{"name":"Molecular Brain Research","volume":"139 2","pages":"Pages 361-366"},"PeriodicalIF":0.0000,"publicationDate":"2005-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.molbrainres.2005.05.032","citationCount":"28","resultStr":"{\"title\":\"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\",\"authors\":\"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\",\"doi\":\"10.1016/j.molbrainres.2005.05.032\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p><span>The effects of HSV-1 amplicon and </span>polyethyleneimine<span><span> (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 </span>Parkinson's disease<span><span>. 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 </span>dopaminergic transmission associated with the degenerative disease.</span></span></p></div>\",\"PeriodicalId\":100932,\"journal\":{\"name\":\"Molecular Brain Research\",\"volume\":\"139 2\",\"pages\":\"Pages 361-366\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2005-10-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/j.molbrainres.2005.05.032\",\"citationCount\":\"28\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular Brain Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0169328X05002524\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Brain Research","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0169328X05002524","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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
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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