{"title":"帕金森病触发内源性神经保护机制:细胞模型研究","authors":"M J Zigmond","doi":"10.1007/978-3-211-45295-0_66","DOIUrl":null,"url":null,"abstract":"<p><p>Glial cell line-derived neurotrophic factor (GDNF) has been implicated in the protection of dopamine (DA) neurons from oxidative stress in animal models of Parkinson's disease (PD). We have now shown that GDNF can also protect against the effects of 6-hydroxydopamine (6-OHDA) in a dopaminergic cell line and in cultures of primary DA neurons prepared from rat substantia nigra (SN). This appears to involve a rapid and transient increase in the phosphorylation of several isoforms of extracellular signal-regulated kinase (ERK). Our evidence indicates that ERK activation also can be modulated by reactive oxygen species (ROS), including those generated by endogenous DA. Identification of the ways by which these pathways can be triggered should provide insights into the pathophysiology of PD, and may offer useful avenues for retarding the progression of the disorder.</p>","PeriodicalId":16395,"journal":{"name":"Journal of Neural Transmission-supplement","volume":" 70","pages":"439-42"},"PeriodicalIF":0.0000,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-211-45295-0_66","citationCount":"16","resultStr":"{\"title\":\"Triggering endogenous neuroprotective mechanisms in Parkinson's disease: studies with a cellular model.\",\"authors\":\"M J Zigmond\",\"doi\":\"10.1007/978-3-211-45295-0_66\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Glial cell line-derived neurotrophic factor (GDNF) has been implicated in the protection of dopamine (DA) neurons from oxidative stress in animal models of Parkinson's disease (PD). We have now shown that GDNF can also protect against the effects of 6-hydroxydopamine (6-OHDA) in a dopaminergic cell line and in cultures of primary DA neurons prepared from rat substantia nigra (SN). This appears to involve a rapid and transient increase in the phosphorylation of several isoforms of extracellular signal-regulated kinase (ERK). Our evidence indicates that ERK activation also can be modulated by reactive oxygen species (ROS), including those generated by endogenous DA. Identification of the ways by which these pathways can be triggered should provide insights into the pathophysiology of PD, and may offer useful avenues for retarding the progression of the disorder.</p>\",\"PeriodicalId\":16395,\"journal\":{\"name\":\"Journal of Neural Transmission-supplement\",\"volume\":\" 70\",\"pages\":\"439-42\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2006-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1007/978-3-211-45295-0_66\",\"citationCount\":\"16\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Neural Transmission-supplement\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1007/978-3-211-45295-0_66\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Neural Transmission-supplement","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-3-211-45295-0_66","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Triggering endogenous neuroprotective mechanisms in Parkinson's disease: studies with a cellular model.
Glial cell line-derived neurotrophic factor (GDNF) has been implicated in the protection of dopamine (DA) neurons from oxidative stress in animal models of Parkinson's disease (PD). We have now shown that GDNF can also protect against the effects of 6-hydroxydopamine (6-OHDA) in a dopaminergic cell line and in cultures of primary DA neurons prepared from rat substantia nigra (SN). This appears to involve a rapid and transient increase in the phosphorylation of several isoforms of extracellular signal-regulated kinase (ERK). Our evidence indicates that ERK activation also can be modulated by reactive oxygen species (ROS), including those generated by endogenous DA. Identification of the ways by which these pathways can be triggered should provide insights into the pathophysiology of PD, and may offer useful avenues for retarding the progression of the disorder.
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