کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4350322 | 1296981 | 2006 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease
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موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease](/preview/png/4350322.png)
چکیده انگلیسی
Altered glutamate transmission in the striatum has been proposed to play a critical role in the pathophysiology of Huntington's disease (HD), a genetic disorder associated with impaired activity of the mitochondrial complex II (succinate dehydrogenase, SD). In the present study, we recorded spontaneous (sEPSCs) and miniature excitatory postsynaptic currents (mEPSCs) from striatal neurons of both toxic (systemic administration of 3-nitropropionic acid in rats) and genetic models of HD (R6/2 transgenic mice). In both models, we found a significant down-regulation of glutamate transmission, suggesting that reduced synaptic excitation of the input structure of the basal ganglia represents a physiological correlate of HD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 410, Issue 1, 13 December 2006, Pages 6-10
Journal: Neuroscience Letters - Volume 410, Issue 1, 13 December 2006, Pages 6-10
نویسندگان
Silvia Rossi, Chiara Prosperetti, Barbara Picconi, Valentina De Chiara, Giorgia Mataluni, Giorgio Bernardi, Paolo Calabresi, Diego Centonze,