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首页> 外文期刊>BMC Neuroscience >Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death
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Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death

机译：慢性NMDA对大鼠给药会增加脑促凋亡因子，同时降低抗凋亡因子并导致细胞死亡

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Background Chronic N -Methyl-D-aspartate (NMDA) administration to rats is reported to increase arachidonic acid signaling and upregulate neuroinflammatory markers in rat brain. These changes may damage brain cells. In this study, we determined if chronic NMDA administration (25 mg/kg i.p., 21 days) to rats would alter expression of pro- and anti-apoptotic factors in frontal cortex, compared with vehicle control. Results Using real time RT-PCR and Western blotting, chronic NMDA administration was shown to decrease mRNA and protein levels of anti-apoptotic markers Bcl-2 and BDNF, and of their transcription factor phospho-CREB in the cortex. Expression of pro-apoptotic Bax, Bad, and 14-3-3ζ was increased, as well as Fluoro-Jade B (FJB) staining, a marker of neuronal loss. Conclusion This alteration in the balance between pro- and anti-apoptotic factors by chronic NMDA receptor activation in this animal model may contribute to neuronal loss, and further suggests that the model can be used to examine multiple processes involved in excitotoxicity.
机译：背景技术据报道，向大鼠长期施用N-甲基-D-天冬氨酸（NMDA）可以增加花生四烯酸信号传导并上调大鼠脑中的神经炎性标志物。这些变化可能会损害脑细胞。在这项研究中，我们确定了与媒介物对照相比，长期给予NMDA（25 mg / kg i.p.，21天）大鼠是否会改变额叶皮层促凋亡和抗凋亡因子的表达。结果显示，通过实时RT-PCR和Western blotting，长期施用NMDA可降低皮质中抗凋亡标记物Bcl-2和BDNF及其转录因子phospho-CREB的mRNA和蛋白质水平。促凋亡的Bax，Bad和14-3-3ζ的表达以及神经元丢失的标志物Fluoro-Jade B（FJB）染色均增加。结论在此动物模型中，慢性NMDA受体激活引起的促凋亡因子和抗凋亡因子之间的平衡变化可能是神经元丢失的原因，并且进一步表明该模型可用于检查涉及兴奋性毒性的多个过程。

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