本文選題：瞬時受體電位通道 + 神經元　； 參考：《中國病理生理雜志》2016年04期

【摘要】：目的:研究瞬時受體電位通道1(TRPC1)缺失對小鼠海馬神經元生存的影響。方法:選用6月齡TRPC1基因敲除小鼠及其對照小鼠,通過神經元特異性標志物Neu N免疫染色、尼氏染色及TUNEL染色檢測TRPC1敲除小鼠海馬CA1、CA3及齒狀回(DG)神經細胞的變化情況。通過Western blot檢測TRPC1基因敲除小鼠促凋亡因子C/EBP同源蛋白(C/EBP homologous protein,CHOP)及凋亡相關蛋白cleaved caspase-3的表達水平。結果:Neu N免疫熒光和尼氏染色發(fā)現,TRPC1基因敲除小鼠海馬CA1、CA3及DG區(qū)神經細胞顯著減少;TUNEL染色檢測發(fā)現TRPC1基因敲除小鼠以上區(qū)域神經細胞凋亡顯著增加;Western blot結果顯示,與對照小鼠相比,TRPC1基因敲除小鼠海馬組織CHOP及cleaved caspase-3的水平均顯著升高。結論:TRPC1基因缺失可導致小鼠海馬神經元數量顯著減少,其機制可能與TRPC1缺失促進神經細胞凋亡有關。
[Abstract]:Aim: to study the effect of the deletion of transient receptor potential channel 1 (TRPC1) on the survival of hippocampal neurons in mice. Methods: 6-month-old TRPC1 knockout mice and their control mice were used to detect the changes of hippocampal CA1mCA3 and dentate gyrus (DGG) neurons in TRPC1 knockout mice by Neu N immunostaining, Nissl staining and Tunel staining. Western blot was used to detect the expression of apoptosis promoting factor C / EBP homologous protein and apoptosis-related protein (cleaved caspase-3) in TRPC1 knockout mice. Results the neuronal cells in the hippocampal CA1pCA3 and DG region of the TRPC1 knockout mice were significantly decreased by using the 10% Neu N immunofluorescence and Nissl staining. The neuronal apoptosis in the above regions of TRPC1 knockout mice was significantly increased by blot. The levels of chop and cleaved caspase-3 in hippocampal tissue of TRPC1 knockout mice were significantly higher than those of control mice. Conclusion the deletion of the 1: TRPC1 gene can significantly decrease the number of hippocampal neurons in mice, and the mechanism may be related to the promotion of neuronal apoptosis by TRPC1 deletion.
【作者單位】： 暨南大學藥學院;深圳市疾病預防控制中心深圳市現代毒理學重點實驗室;
【基金】：廣東省自然科學基金資助項目(No.2014A030313715) 深圳市科技研發(fā)基金基礎研究項目(No.JCYJ20130329103949650)
【分類號】：R363

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