کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4347637 | 1296852 | 2009 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Silencing of ZnT1 reduces Zn2+ efflux in cultured cortical neurons
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موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Zinc dyshomeostasis in brain might be involved in the pathogenesis of a series of brain diseases such as Alzheimer's disease and stroke. It is essential that the level of intracellular free Zn2+ in neurons is tightly controlled to maintain a narrow window of optimal concentration. The plasma membrane bound transporter ZnT1 is suggested to lower intracellular Zn2+ concentration. In this study, the function of ZnT1 in cultured cortical neurons was studied. Using vector-based shRNA interference, the expression of this protein was reduced approximately 40% in cultured rat cortical neurons when measured by immunofluorescence using a ZnT1 antibody. Changes in intracellular Zn2+ levels were tracked in individual neurons by microfluorometry using the Zn2+ selective fluorophore, FluoZin3. Unopposed Zn2+ efflux was measured by first loading cultured cortical neurons with Zn2+ then reducing extracellular Zn2+ to near zero by addition of EDTA. Reducing ZnT1 expression caused Zn2+ efflux to decrease compared with the Zn2+ efflux measured in nonsense transfected neurons, suggesting that ZnT1 plays a direct role in Zn2+ efflux. ZnT1 dependent Zn2+ efflux rate was higher in the first 10Â min than at later time periods suggesting that ZnT1-mediated efflux was heavily dependent on the intracellular free Zn2+ concentration and/or required an outwardly directed Zn2+ gradient.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 450, Issue 2, 30 January 2009, Pages 206-210
Journal: Neuroscience Letters - Volume 450, Issue 2, 30 January 2009, Pages 206-210
نویسندگان
Yan Qin, Dustin Thomas, Charles P. Fontaine, Robert A. Colvin,