کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6272890 | 1614792 | 2015 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Presynaptic cell type-dependent regulation of GABAergic synaptic transmission by nitric oxide in rat insular cortex
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کلمات کلیدی
PPRNMDAN-methyl-d-aspartatenNOSNO synthaseNADPH-dLTSfast-spiking interneuronVGATPBSPKGpresynapticpostsynapticPYRODQ3-3′-diaminobenzidineS-nitroso-N-acetyl-dl-penicillamineVDCCsDABaCSFpKaHEPESCTANOSEGTAcGMPBSA - BSAN-(2-Hydroxyethyl)piperazine-N′-2-ethanesulfonic acid - N- (2-Hydroxyethyl) piperazine-N'-2-ethanesulfonic acidPTIO - ptiobovine serum albumin - آلبومین سرم گاوethylene glycol tetraacetic acid - اتیلن گلیکول تتراستیک اسیدTRIS buffer - بافر TRISphosphate buffer - بافر فسفاتConditioned taste aversion - بی نظمی طعم و مزهvesicular GABA transporter - حامل ویسکوزر GABANADPH diaphorase - دیافرااز NADPHPyramidal cell - سلول پیرامیدSNAP - ضربه محکم و ناگهانیinsular cortex - قشر ساحلیartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریcyclic guanosine monophosphate - مونوفسفات گوانوزین چرخه ایpaired-pulse ratio - نسبت پالس زوجNeuronal NO synthase - نیاسین سنتاز NONitric oxide - نیتریک اکسیدParvalbumin - پاروالبومینprotein kinase A - پروتئین کیناز Aprotein kinase G - پروتئین کیناز GWhole-cell patch-clamp - پچ-کلمپ کل سلولVoltage-dependent calcium channels - کانال های کلسیم وابسته به ولتاژGABA - گاباguanylyl cyclase - گویینیل سیکلاس
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Nitric oxide (NO) is a key retrograde messenger that regulates synaptic transmission in the cerebral cortex. However, little is known about NO-induced modulatory effects and their mechanisms relative to inhibitory synaptic transmission. The present study aimed to examine the effects of NO on unitary inhibitory postsynaptic currents (uIPSCs) and to postulate the synaptic location of NO action. We performed multiple whole-cell patch-clamp recordings from rat insular cortex and divided recorded cells into three subtypes: pyramidal cells (Pyr), fast-spiking interneurons (FS), and non-FS GABAergic interneurons. In the connections from FS to Pyr (FS â Pyr), the application of S-nitroso-N-acetyl-dl-penicillamine (SNAP, 100 μM), an NO donor, suppressed uIPSC amplitudes in 31% of the connections, whereas 39% of the connections showed uIPSC facilitation. The remaining FS â Pyr connections showed little effect of SNAP on uIPSCs. An analysis of paired-pulse ratio (PPR) implied the involvement of presynaptic mechanisms in SNAP-induced effects on uIPSCs. Similar effects of SNAP were observed in FS â FS/non-FS connections; 33%, 54%, and 13% of the connections were facilitated, suppressed, and unchanged, respectively. In contrast, non-FS â Pyr or FS/non-FS showed constant uIPSC suppression by SNAP. PPR analysis supports the hypothesis that these SNAP-induced effects are mediated by presynaptic mechanisms in FS â FS/non-FS and non-FS â Pyr/FS/non-FS connections. The NO scavenger, 2-phenyl-4,4,5,5-tetramethylimidazolineoxyl-1-oxyl-3-oxide (PTIO), or the inhibitor of guanylate cyclase, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), abolished the SNAP-induced uIPSC modulation. These results suggest that NO regulation of inhibitory synaptic transmission is dependent on presynaptic cell subtypes and that, at least in part, the effects are mediated by presynaptic mechanisms.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 284, 22 January 2015, Pages 65-77
Journal: Neuroscience - Volume 284, 22 January 2015, Pages 65-77
نویسندگان
K. Yamamoto, H. Takei, Y. Koyanagi, N. Koshikawa, M. Kobayashi,