کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6021445 | 1580637 | 2016 | 48 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Effects of L-dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of Parkinson's disease
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
8-OH-DPATFTGGlobus pallidus internal segmentSKF81297Repeated-measuresBenserazideALODPATGPiLFPSTN5-HTSNR6-OHDARMSFFT6-Hydroxydopaminei.p.l-DOPA - L-DOPAPCA - PCAAIMS - اهدافParkinson's disease - بیماری پارکینسونPrincipal component analysis - تحلیل مولفههای اصلی یا PCAsubstantia nigra - توده سیاهabnormal involuntary movements - حرکات غیر دائمی غیر طبیعیIntraperitoneally - داخل صفاقیDopamine - دوپامینSerotonin - سروتونینlevodopa - لوودوپاroot mean square - میانگین مربع ریشهSignal-to-noise ratio - نسبت سیگنال به نویزSubthalamic nucleus - هسته ی زیرهالامیکlocal field potential - پتانسیل منطقه ایQuinpirole - کینپیرول
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Effects of L-dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of Parkinson's disease Effects of L-dopa priming on cortical high beta and high gamma oscillatory activity in a rodent model of Parkinson's disease](/preview/png/6021445.png)
چکیده انگلیسی
Prolonged L-dopa treatment in Parkinson's disease (PD) often leads to the expression of abnormal involuntary movements known as L-dopa-induced dyskinesia. Recently, dramatic 80Â Hz oscillatory local field potential (LFP) activity within the primary motor cortex has been linked to dyskinetic symptoms in a rodent model of PD and attributed to stimulation of cortical dopamine D1 receptors. To characterize the relationship between high gamma (70-110Â Hz) cortical activity and the development of L-dopa-induced dyskinesia, cortical LFP and spike signals were recorded in hemiparkinsonian rats treated with L-dopa for 7Â days, and dyskinesia was quantified using the abnormal involuntary movements (AIMs) scale. The relationship between high gamma and dyskinesia was further probed by assessment of the effects of pharmacological agents known to induce or modulate dyskinesia expression. Findings demonstrate that AIMs and high gamma LFP power increase between days 1 and 7 of L-dopa priming. Notably, high beta (25-35Â Hz) power associated with parkinsonian bradykinesia decreased as AIMs and high gamma LFP power increased during priming. After priming, rats were treated with the D1 agonist SKF81297 and the D2 agonist quinpirole. Both dopamine agonists independently induced AIMs and high gamma cortical activity that were similar to that induced by L-dopa, showing that this LFP activity is neither D1 nor D2 receptor specific. The serotonin 1A receptor agonist 8-OH-DPAT reduced L-dopa- and DA agonist-induced AIMs and high gamma power to varying degrees, while the serotonin 1A antagonist WAY100635 reversed these effects. Unexpectedly, as cortical high gamma power increased, phase locking of cortical pyramidal spiking to high gamma oscillations decreased, raising questions regarding the neural substrate(s) responsible for high gamma generation and the functional correlation between high gamma and dyskinesia.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 86, February 2016, Pages 1-15
Journal: Neurobiology of Disease - Volume 86, February 2016, Pages 1-15
نویسندگان
Kristin B. Dupre, Ana V. Cruz, Alex J. McCoy, Claire Delaville, Colin M. Gerber, Katherine W. Eyring, Judith R. Walters,