alterations in mglur5 expression and signaling in lewy body disease and in transgenic models of alpha-synucleinopathy – implications for excitotoxicity改变受体表达和信号在路易身体疾病和转基因模型alpha-synucleinopathyu2014u2014会影响.pdfVIP

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2017-09-07 发布于上海
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alterations in mglur5 expression and signaling in lewy body disease and in transgenic models of alpha-synucleinopathy – implications for excitotoxicity改变受体表达和信号在路易身体疾病和转基因模型alpha-synucleinopathyu2014u2014会影响.pdf

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alterations in mglur5 expression and signaling in lewy body disease and in transgenic models of alpha-synucleinopathy – implications for excitotoxicity改变受体表达和信号在路易身体疾病和转基因模型alpha-synucleinopathyu2014u2014会影响

Alterations in mGluR5 Expression and Signaling in Lewy Body Disease and in Transgenic Models of Alpha- Synucleinopathy – Implications for Excitotoxicity 1,3¤ 1 1 3,4 3,4 Diana L. Price , Edward Rockenstein , Kiren Ubhi , Van Phung , Natalie MacLean-Lewis , David 1,3 1 1 1 1 1,3,4 Askay , Anna Cartier , Brian Spencer , Christina Patrick , Paula Desplats , Mark H. Ellisman , Eliezer Masliah1,2* 1 Department of Neurosciences, University of California San Diego, La Jolla, California, United States of America, 2 Department of Pathology, University of California San Diego, La Jolla, California, United States of America, 3 National Center for Microscopy and Imaging Research, University of California San Diego, La Jolla, California, United States of America, 4 Center for Research in Biological Systems, University of California San Diego, La Jolla, California, United States of America Abstract Dementia with Lewy bodies (DLB) and Parkinson’s Disease (PD) are neurodegenerative disorders of the aging population characterized by the abnormal accumulation of alpha-synuclein (alpha-syn). Previous studies have suggested that excitotoxicity may contribute to neurodegeneration in these disorders, however the underlying mechanisms and their relationship to alpha-syn remain unclear. For this study we proposed that accumulation of alpha-syn might result in alterations in metabotropic glutamate receptors (mGluR), particularly mGluR5 which has been linked to deficits in murine models of PD. In this contex