کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6270816 | 1614744 | 2016 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Activation of the sigma receptor 1 modulates AMPA receptor-mediated light-evoked excitatory postsynaptic currents in rat retinal ganglion cells
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کلمات کلیدی
MK-801KT5720PPRNMDARPKCPKGU73122SKFPLCPI-PLCKT5823TTXpKaAMPAREGTAHEPESGö69764-(2-hydroxyethyl)-1-piperazineethanesulfonic acid - 4- (2-hydroxyethyl) -1-piperazineethanesulfonic acidBiP - BIPDMSO - DMSOPhosphatidylinositol-specific phospholipase C - Fosfatidylinositol خاص فسفولیپاز C[Ca2+]i - [Ca2 +] iethylene glycol tetraacetic acid - اتیلن گلیکول تتراستیک اسیدNeurotransmission - انتقال عصبیtetrodotoxin - تترو دوتوکسین excitatory postsynaptic current - جریان پستیینپتیک تحریک کنندهdizocilpine - دیسلوکپیپینDimethyl sulfoxide - دیمتیل سولفواکسیدganglion cell - سلول گانگلیونیRetina - شبکیهintracellular calcium concentration - غلظت کلسیم داخل سلولیphospholipase C - فسفولیپاز Cpaired-pulse ratio - نسبت پالس زوجBinding immunoglobulin Protein - پروتئین ایمونوگلوبولین Bindingprotein kinase A - پروتئین کیناز Aprotein kinase G - پروتئین کیناز GProtein kinase C - پروتئین کیناز سیAMPA receptor - گیرنده AMPAN-methyl-d-aspartate receptor - گیرنده N-methyl-d-aspartateSigma receptor - گیرنده سیگما
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Sigma receptor (ÏR), a unique receptor family, is classified into three subtypes: ÏR1, ÏR2 and ÏR3. It was previously shown that ÏR1 activation induced by 1 μM SKF10047 (SKF) suppressed N-methyl-d-aspartate (NMDA) receptor-mediated responses of rat retinal ganglion cells (GCs) and the suppression was mediated by a distinct Ca2+-dependent phospholipase C (PLC)-protein kinase C (PKC) pathway. In the present work, using whole-cell patch-clamp techniques in rat retinal slice preparations, we further demonstrate that SKF of higher dosage (50 μM) significantly suppressed AMPA receptor (AMPAR)-mediated light-evoked excitatory postsynaptic currents (L-EPSCs) of retinal ON-type GCs (ON GCs), and the effect was reversed by the ÏR1 antagonist BD1047, suggesting the involvement of ÏR1. The SKF (50 μM) effect was unlikely due to a change in glutamate release from bipolar cells, as suggested by the unaltered paired-pulse ratio (PPR) of AMPAR-mediated EPSCs of ON GCs. SKF (50 μM) did not change L-EPSCs of ON GCs when the G protein inhibitor GDP-β-S or the protein kinase G (PKG) inhibitor KT5823 was intracellularly infused. Calcium imaging further revealed that SKF (50 μM) did not change intracellular calcium concentration in GCs and persisted to suppress L-EPSCs when intracellular calcium was chelated by BAPTA. The SKF (50 μM) effect was intact when protein kinase A (PKA) and phosphatidylinostiol (PI)-PLC signaling pathways were both blocked. We conclude that the SKF (50 μM) effect is Ca2+-independent, PKG-dependent, but not involving PKA, PI-PLC pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 332, 22 September 2016, Pages 53-60
Journal: Neuroscience - Volume 332, 22 September 2016, Pages 53-60
نویسندگان
Lei-Lei Liu, Qin-Qin Deng, Shi-Jun Weng, Xiong-Li Yang, Yong-Mei Zhong,