4-hydroxynonenal modulates the long-term potentiation induced by L-type Ca2+ channel activation in the rat dentate gyrus in vitro
4-hydroxynonenal modulates the long-term potentiation induced by L-type Ca2+ channel activation in the rat dentate gyrus in vitro
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DOI：
10.1016/j.neulet.2004.08.015
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发表时间：
2004-11-11
影响因子：
2.5
通讯作者：
Ito, Y
中科院分区：
文献类型：
--
作者：
Akaishi, T;Nakazawa, K;Ito, Y
在神经元的生理和变性条件下，氧自由基产生和膜脂质过氧化（MLP）增加。我们研究了膜脂质过氧化产物4-羟基壬烯醛（4 HN）是否影响离体大鼠齿状回的长时程增强（LTP）。用4 HN（10 μ M）处理海马切片增强UP而不影响基础诱发电位。2 μ M硝苯地平可完全抑制这种增强作用，硝苯地平是一种L型钙通道阻滞剂。在培养的齿状回神经元中，用4 HN处理细胞24小时导致大量细胞死亡，这些细胞死亡被谷胱甘肽解毒，而用4 HN短期处理（小于或等于6小时）则没有影响。硝苯地平部分但显著抑制4 HN诱导的细胞死亡。这些结果表明，4 HN调节LTP和诱导迟发性细胞死亡，通过L-型Ca 2+通道激活齿状回。因此，4 HN在海马的生理和病理生理事件中起重要作用。(C)2004爱思唯尔爱尔兰有限公司保留所有权利。
Increased oxyradical production and membrane lipid peroxidation (MLP) occur under physiological and degenerative conditions in neurons. We investigated whether 4-hydroxynonenal (4HN), one of the membrane lipid peroxidation products, affects long-term potentiation (LTP) in the rat dentate gyrus in vitro. Treatment of hippocampal slices with 4HN (10 muM) enhanced UP without affecting basal evoked potentials. The enhancement was completely inhibited by 2 muM nifedipine, a blocker of L-type Ca2+ channels. In cultured dentate gyrus neurons, treatment of the cells with 4HN for 24 h resulted in a significant amount of cell death that was detoxified by glutathione, whereas short-term treatment with 4HN (less than or equal to6 h) had no effect. Nifedipine partially but significantly suppressed the 4HN-induced cell death. These results suggest that 4HN modulates LTP and induces delayed cell death through L-type Ca2+ channel activation in the dentate gyrus. 4HN thereby plays an important role in both physiological and pathophysiological events in the hippocampus. (C) 2004 Elsevier Ireland Ltd. All rights reserved.