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首页> 外文期刊>The European Journal of Neuroscience >COX-2, but not COX-1, activity is necessary for the induction of perforant path long-term potentiation and spatial learning in vivo.
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COX-2, but not COX-1, activity is necessary for the induction of perforant path long-term potentiation and spatial learning in vivo.

机译：COX-2活性而不是COX-1活性对于诱导穿孔路径长期增强和体内空间学习是必需的。

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The objectives of this research were to investigate the role played by the enzyme cyclooxygenase (COX) in learning and memory, synaptic plasticity and synaptic transmission in the rat brain in vivo. Male Wistar rats were treated with isoform-selective inhibitors for COX-1 and COX-2, either chronically and tested in the watermaze or acutely before electrophysiological recordings were made. We found a significant impairment in acquisition of the watermaze with inhibition of COX-2. Furthermore, we found COX-2 but not COX-1 inhibition significantly blocked long-term potentiation (LTP) induction but had no effect on already established LTP. Moreover, exogenous replacement of the main metabolite of COX-2 activity, PGE(2), was sufficient to restore LTP induction and for normal downstream signalling to ensue, namely extracellular signalling-regulated kinase (ERK)-phosphorylation and c-FOS expression. We conclude that endogenous basal levels of PGE(2) resulting from COX-2 but not COX-1 activity are necessary for synaptic plasticity and memory acquisition.
机译：这项研究的目的是调查环氧化酶（COX）在体内大鼠大脑的学习和记忆，突触可塑性和突触传递中的作用。长期对雄性Wistar大鼠进行COX-1和COX-2的同种型选择性抑制剂治疗，并在进行电生理记录之前先在水迷宫中或对其进行急性测试。我们发现在抑制COX-2的情况下，获取水迷宫存在重​​大障碍。此外，我们发现COX-2的抑制作用而不是COX-1的抑制作用显着阻止了长期增强（LTP）的诱导，但对已经建立的LTP没有影响。此外，COX-2活性的主要代谢物PGE（2）的外源替代足以恢复LTP诱导并确保正常的下游信号传导，即细胞外信号传导激酶（ERK）磷酸化和c-FOS表达。我们得出结论，内源性基础水平的PGE（2）由COX-2产生，但不是COX-1活性对于突触可塑性和记忆获得是必需的。

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