کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4342468 | 1295870 | 2007 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Noradrenergic modulation of the hyperpolarization-activated cation current (Ih) in dopamine neurons of the ventral tegmental area
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
DRGPKCEGTASNCaCSFVTAMNTBdorsal root ganglion - گانگلیون ریشه پشتیanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceDopamine - دوپامینartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیSubstantia nigra compacta - متراکم توده سیاهventral tegmental area - ناحیه تگمنتوم شکمیnorepinephrine - نوراپی نفرینmedial nucleus of the trapezoid body - هسته مرکزی بدن تراپزیProtein kinase C - پروتئین کیناز سیAdrenergic receptors - گیرنده های آدرنرژیکDopamine receptors - گیرنده های دوپامین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Alterations in the state of excitability of midbrain dopamine (DA) neurons from the ventral tegmental area (VTA) may underlie changes in the synaptic plasticity of the mesocorticolimbic system. Here, we investigated norepinephrine's (NE) regulation of VTA DA cell excitability by modulation of the hyperpolarization-activated cation current, Ih, with whole cell recordings in rat brain slices. Current clamp recordings show that NE (40 μM) hyperpolarizes spontaneously firing VTA DA cells (11.23±4 mV; n=8). In a voltage clamp, NE (40 μM) induces an outward current (100±24 pA; n=8) at â60 mV that reverses at about the Nernst potential for potassium (â106 mV). In addition, NE (40 μM) increases the membrane cord conductance (179±42%; n=10) and reduces Ih amplitude (68±3% of control at â120 mV; n=10). The noradrenergic α-1 antagonist prazosin (40 μM; n=5) or the α-2 antagonist yohimbine (40 μM; n=5) did not block NE effects. All NE-evoked events were blocked by the D2 antagonists sulpiride (1 μM) and eticlopride (100 nM) and no significant reduction of Ih took place in the presence of the potassium channel blocker BaCl2 (300 μM). Therefore, it is concluded that NE inhibition of Ih was due to an increase in membrane conductance by a nonspecific activation of D2 receptors that induce an outward potassium current and is not a result of a second messenger system acting on h-channels. The results also suggest that Ih channels are mainly located at dendrites of VTA DA cells and, thus, their inhibition may facilitate the transition from single-spike firing to burst firing and vice versa.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 149, Issue 2, 26 October 2007, Pages 303-314
Journal: Neuroscience - Volume 149, Issue 2, 26 October 2007, Pages 303-314
نویسندگان
F. Arencibia-Albite, C. Paladini, J.T. Williams, C.A. Jiménez-Rivera,