کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6262591 | 1613805 | 2016 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Suppression of outward K+ currents by activating dopamine D1 receptors in rat retinal ganglion cells through PKA and CaMKII signaling pathways
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کلمات کلیدی
TTXRITCLarge-conductance Ca2+-activated K+ channelsKATPPKCPLC4-APpKaCaMKIIRGCERKEGTAHEPES4-(2-Hydroxyethyl)piperazine-1-ethanesulfonic acid - 4- (2-Hydroxyethyl) piperazine-1-ethanesulfonic acid4-aminopyridine - 4-آمینوپیریدینBKCa - BKC بهDMSO - DMSOMAPK - MAPKadenylate cyclase - آدنیلات سیکلاسTetraethylammonium - تترا اتیل آمونیومtetrodotoxin - تترو دوتوکسین CNS - دستگاه عصبی مرکزیDopamine - دوپامینDimethyl sulfoxide - دیمتیل سولفواکسیدretinal ganglion cell - سلول گانگلیونی شبکیهcentral nervous system - سیستم عصبی مرکزیphospholipase C - فسفولیپاز Cprotein kinase A - پروتئین کیناز Acalcium/calmodulin-dependent protein kinase II - پروتئین کیناز II وابسته به کلسیم / کالودولینProtein kinase C - پروتئین کیناز سیmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenPatch-clamp - پچ گیرTEA - چایATP-sensitive K+ channels - کانال های K + حساس به ATPextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیGlybenclamide - گلیبن کلامیدDopamine D1 receptor - گیرنده Dopamine D1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Dopamine plays an important role in regulating neuronal functions in the central nervous system by activating the specific G-protein coupled receptors. Both D1 and D2 dopamine receptors are extensively distributed in the retinal neurons. In the present study, we investigated the effects of D1 receptor signaling on outward K+ currents in acutely isolated rat retinal ganglion cells (RGCs) by patch-clamp techniques. Extracellular application of SKF81297 (10 μM), a specific D1 receptor agonist, significantly and reversibly suppressed outward K+ currents of the cells, which was reversed by SCH23390 (10 μM), a selective D1 receptor antagonist. We further showed that SKF81297 mainly suppressed the glybenclamide (Gb)- and 4-aminopyridine (4-AP)-sensitive K+ current components, but did not show effect on the tetraethylammonium (TEA)-sensitive one. Both protein kinase A (PKA) and calcium/calmodulin-dependent protein kinase II (CaMKII) signaling pathways were likely involved in the SKF81297-induced suppression of the K+ currents since either Rp-cAMP (10 μM), a cAMP/PKA signaling inhibitor, or KN-93 (10 μM), a specific CaMKII inhibitor, eliminated the SKF81297 effect. In contrast, neither protein kinase C (PKC) nor mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) signaling pathway seemed likely to be involved because both the PKC inhibitor bisindolylmaleimide IV (Bis IV) (10 μM) and the MAPK/ERK1/2 inhibitor U0126 (10 μM) did not block the SKF81297-induced suppression of the K+ currents. These results suggest that activation of D1 receptors suppresses the Gb- and 4-AP-sensitive K+ current components in rat RGCs through the intracellular PKA and CaMKII signaling pathways, thus modulating the RGC excitability.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1635, 15 March 2016, Pages 95-104
Journal: Brain Research - Volume 1635, 15 March 2016, Pages 95-104
نویسندگان
Qian Li, Na Wu, Peng Cui, Feng Gao, Wen-Jing Qian, Yanying Miao, Xing-Huai Sun, Zhongfeng Wang,