کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4339387 | 1295752 | 2010 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Postsynaptic density-93 deficiency protects cultured cortical neurons from N-methyl-d-aspartate receptor-triggered neurotoxicity
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کلمات کلیدی
nNOSmembrane-associated guanylate kinasesMAGUKswide-typeNMDARPSD-93cGMPshRNAPSD3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide - 3- (4،5-dimethylthiazol-2-yl) -2،5-difenyltetrazolium bromide6-Cyano-7-nitroquinoxaline-2,3-dione - 6-Cyano-7-nitroquinoxaline-2،3-dionel-NAME - L-NAMEMTT - MTTsmall hairpin RNA - RNA کوچک موی سرpostsynaptic density - تراکم Postinapticneuronal nitric oxide synthase - سنتاز اکسید نیتریک عصبیCNQX - سیانکیوایکسknockout - ناکاوتNitric oxide - نیتریک اکسیدnitric oxide synthase - نیتریک اکسید سنتازPropidium iodide - پروتئین یدیدcyclic guanosine 3′,5′-monophosphate - گوانوزین سیکل 3 '، 5'-مونوفسفرهN-methyl-d-aspartate receptor - گیرنده N-methyl-d-aspartateN-Methyl-d-aspartate receptors - گیرنده های N-methyl-d-aspartate
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Postsynaptic density-93 deficiency protects cultured cortical neurons from N-methyl-d-aspartate receptor-triggered neurotoxicity Postsynaptic density-93 deficiency protects cultured cortical neurons from N-methyl-d-aspartate receptor-triggered neurotoxicity](/preview/png/4339387.png)
چکیده انگلیسی
It has been reported that N-methyl-d-aspartate receptor (NMDAR)-triggered neurotoxicity is related to excessive Ca2+ loading and an increase in nitric oxide (NO) concentration. However, the molecular mechanisms that underlie these events are not completely understood. NMDARs and neuronal NO synthase each binds to the scaffolding protein postsynaptic density (PSD)-93 through its PDZ domains. In this study, we determined whether PSD-93 plays a critical role in NMDAR/Ca2+/NO-mediated neurotoxicity. We found that the targeted disruption of the PSD-93 gene attenuated the neurotoxicity triggered by NMDAR activation, but not by non-NMDAR activation, in cultured mouse cortical neurons. PSD-93 deficiency reduced the amount of NMDAR subunits NR2A and NR2B in synaptosomal fractions from the cortical neurons and significantly prevented NMDA-stimulated increases in cyclic guanosine 3â²,5â²-monophosphate and Ca2+ loading in the cortical neurons. These findings indicate that PSD-93 deficiency could block NMDAR-triggered neurotoxicity by disrupting the NMDAR-Ca2+-NO signaling pathway and reducing expression of synaptic NR2A and NR2B. Since NMDARs, Ca2+, and NO play a critical role during the development of brain trauma, seizures, and ischemia, the present work suggests that PSD-93 might contribute to molecular mechanisms of neuronal damage in these brain disorders.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 166, Issue 4, 14 April 2010, Pages 1083-1090
Journal: Neuroscience - Volume 166, Issue 4, 14 April 2010, Pages 1083-1090
نویسندگان
M. Zhang, J.T. Xu, X. Zhu, Z. Wang, X. Zhao, Z. Hua, Y.X. Tao, Y. Xu,