کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4350910 1296999 2006 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
NMDA receptor/L-VGCC-dependent expression and AMPA/KA receptor-dependent activation of c-Jun induced by cerebral ischemia in rat hippocampus
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
NMDA receptor/L-VGCC-dependent expression and AMPA/KA receptor-dependent activation of c-Jun induced by cerebral ischemia in rat hippocampus
چکیده انگلیسی
Over-activation of ionotropic glutamate receptors can cause an excessive influx of calcium ions into neurons, which subsequently triggers the degeneration and death of cells in a process known as excitotoxicity. Here, we examined the effects of modulating ionotropic glutamate receptors and L-type voltage-gated calcium channels (L-VGCC) on the expression and activation of c-Jun in hippocampus of SD rats after transient global ischemia. The total protein of c-Jun was altered by ischemia-reperfusion and reached its high levels at 3-6 h of reperfusion. However, the increased expression was prevented by pretreatment of ketamine (a non-competitive N-methyl-d-aspartate (NMDA) receptors antagonist) or nifedipine (a blocker of L-VGCC), but not by 6,7-dinitroquinoxaline-2,3(1H,4H)-dione (DNQX), an AMPA/KA receptor antagonist. On the other hand, c-Jun phosphorylation was significantly increased 3 h after reperfusion, which was inhibited by DNQX, but not ketamine or nifedipine. AP-1 binding activity reactions were also performed by electrophoretic mobility shift assay (EMSA), which detected similar results as those in Western blotting. Our results clearly showed that c-Jun expression is NMDA receptor/L-VGCC-dependent and c-Jun activation is AMPA/KA receptor-dependent, which expands our knowledge of the JNK-c-Jun signaling pathway in ischemic brain damage.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 398, Issue 3, 8 May 2006, Pages 268-273
نویسندگان
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