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Effects of calcium channel on 3-morpholinosydnonimine-induced rat hippocampal neuronal apoptosis

查看全文 作  者:Quanzhong [1]Chang;Shuling [2]Zhang;Yuanyin [1]Zheng;Lijuan [1]Xu;Jinbao [1]Yin;Shining [1]Cai 高影响力作者 机构地区:[1]Department of Physiology, Zhuhai Campus of Zunyi Medical College, Zhuhai 519041, Guangdong Province, China;[2]Department of Pediatrics, Zh uhai Campus of Zunyi Medical College, Zhuhai 519041, Guangdong Pro vince, China高影响力机构 出  处:《Neural Regeneration Research》索引2011年第6卷第5期,共5页高影响力期刊 基  金:Supported by the Science and Technology Department of Guizhou Province, No. C20072127, SY20093075;the Science and Technology Department of Zhuhai City, No. PC20081010 摘  要:Previous studies have demonstrated that increased chloride channel activity plays a role in nitric oxide-induced neuronal apoptosis in the rat hippocampus. The present study investigated the effects of the broad-spectrum calcium channel blocker CdCl2 on survival rate, percentage of apoptosis, and morphological changes in hippocampal neurons cultured in vitro, as well as the effects of calcium channels on neuronal apoptosis. The chloride channel blockers 4-acetamido-4'-isothiocyanatostilbene-2, 2'-disulfonic acid (SITS) or 4, 4'-diisothiocyanostilbene-2, 2'-disulfonic acid (DIDS) increased the survival rate of 3-morpholinosydnonimine (SIN-1)-treated neurons and suppressed SIN-1-induced neuronal apoptosis. The calcium channel blocker CdCl2 did not increase the survival rate of neurons and did not affect SIN-1-induced apoptosis or SITS- or DIDS-suppressed neuronal apoptosis. Results demonstrated that calcium channels did not significantly affect neuronal apoptosis. 关 键 词:神经细胞凋亡 钙通道阻滞剂 海马神经元 诱导 分布式入侵检测系统 大鼠 氯离子通道 形态学变化
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