کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5502889 | 1535086 | 2017 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Sigma-1 receptor in brain ischemia/reperfusion: Possible role in the NR2A-induced pathway to regulate brain-derived neurotrophic factor
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کلمات کلیدی
CREBLSDbFGFCNTFERKBCCAoCaMKIVBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز bilateral common carotid artery occlusion - دو طرفه انسداد شریان کاروتید مشترکendoplasmic reticulum - شبکه آندوپلاسمی basic fibroblast growth factor - فاکتور رشد فیبروبلاست پایهBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزciliary neurotrophic factor - فاکتور نوروتروفیک ciliaryknockout - ناکاوتcyclic AMP response element-binding protein - پروتئین اتصال دهنده عنصر Response Cyclic AMP
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Sigma-1 receptor (Ï1r) activation could attenuate the learning and memory deficits in the AD model, ischemia model and others. In our previous study, the activation of Ï1r increased the expression of brain-derived neurotrophic factor (BDNF), possibly through the NR2A-induced pathway, and Ï1r agonists might function as neuroprotectant agents in vascular dementia. Here, we used Ï1r knockout mice to confirm the role of Ï1r. Furthermore, an antagonist of NR2A was first used to investigate whether the NR2A-induced pathway is the necessary link between Ï1r and BDNF. The operation of brain ischemia/reperfusion was induced by bilateral common carotid artery occlusion for 20 min in C57BL/6 and Ï1r knockout mice as the ischemic group. A Ï1r agonist, PRE084 (1 mg/kg, i.p.), and NR2A antagonist, PEAQX (10 mg/kg, i.p.), were administered once daily throughout the experiment. Behavioral tests were performed starting on day 8. On day 22 after brain ischemia/reperfusion, mice were sacrificed and brains were immediately collected and the injured and the hippocampus was isolated and stored at â 80 °C for western blot analysis. After ischemic operation, contrast with the Ï1r knockout mice, PRE084 significantly ameliorated learning and memory impairments in the behavioral evaluation, and prevented the protein decline of BDNF, NR2A, CaMKIV and TORC1 expression in wild-type mice. However, the effects of PRE084 on CaMKIV-TORC1-CREB and BDNF, even for learning and memory impairment, were antagonized by the co-administration of PEAQX, an antagonist of NR2A. The activation of Ï1r improves the impairment of learning and memory in the ischemia/reperfusion model, and the expression of BDNF, which may have been achieved through the NR2A-CaMKIV-TORC1 pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of the Neurological Sciences - Volume 376, 15 May 2017, Pages 166-175
Journal: Journal of the Neurological Sciences - Volume 376, 15 May 2017, Pages 166-175
نویسندگان
Qian Xu, Xue-Fei Ji, Tian-Yan Chi, Peng Liu, Ge Jin, Ling Chen, Li-Bo Zou,