کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4339514 | 1295758 | 2010 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Fcγ receptors contribute to pyramidal cell death in the mouse hippocampus following local kainic acid injection
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کلمات کلیدی
iNOSC57BL/6NFcRγFcγRsN-methyl-d-aspartateNMDAMMP-2DABCOX-2tPAPVDFFITCPBSkainic acid - اسید کرییکpolyvinylidene difluoride - دی فلوئورید پلی وینیلیدینinducible nitric-oxide synthase - سنتاز نیتریک اکسید القاییCyclooxygenase-2 - سیکلوکوکسیژناز2Phosphate buffered saline - فسفات بافر شورtissue plasminogen activator - فعال کننده بافتی پلاسمینوژنfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتMatrix metalloproteinase-2 - ماتریکس متالوپروتئیناز-2Parvalbumin - پاروالبومین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Recent studies have demonstrated the contribution of the gamma subunit of the Fc receptor of IgG (FcRγ) to neuronal death following ischemic injury and Parkinson's disease. We examined the role of FcRγ in hippocampal pyramidal cell death induced by kainic acid (KA). FcRγ-deficient mice (FcRγâ/â) and their FcRγ+/+ littermates (wild type, B6) received an injection of KA into the dorsal hippocampus. Pyramidal cell death was quantified 24 and 72 h after the injection. The number of survived pyramidal cells was significantly larger in FcRγâ/â mice than in B6 mice in both the CA1 and CA3. Immunohistochemical and immunofluorescent studies detected FcγRIIB protein in parvalbumin neurons, whereas FcγRIII and FcγRI proteins were detected in microglial cells. No activated microglial cells were detected 24 h after the KA injection in FcRγâ/â mice, whereas many activated microglial cells were present in B6 mice. The production of nitrotyrosine as well as of the inducible nitric oxide synthase and cyclooxygenase-2 proteins, increased by 16 h after the KA injection in B6 mice. In addition, tissue plasminogen activator and metalloproteinase-2 proteins increased. By contrast, the magnitude of oxidative stress and the increase in protease expression were mild in FcRγâ/â mice. Co-injection of a neutralizing antibody against FcγRll and FcγRlll with KA abolished pyramidal cell death and microglial activation. In addition, the neutralizing antibody reduced oxidative stress and expression of proteases. These observations suggested a role for FcγRllB in parvalbumin neurons as well as FcRγ in microglia in pyramidal cell death.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 166, Issue 3, 31 March 2010, Pages 819-831
Journal: Neuroscience - Volume 166, Issue 3, 31 March 2010, Pages 819-831
نویسندگان
S. Suemitsu, M. Watanabe, E. Yokobayashi, S. Usui, T. Ishikawa, Y. Matsumoto, N. Yamada, M. Okamoto, S. Kuroda,