Bifemelane protects cultured cortical neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity.
Bifemelane protects cultured cortical neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity.
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Bifemelane 保护培养的皮质神经元免受 N-甲基-D-天冬氨酸受体介导的谷氨酸细胞毒性。
DOI：
10.1254/jjp.76.313
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
S. Kaneko
中科院分区：
文献类型：
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作者：
A. Akaike;T. Maeda;T. Kume;S. Kaneko
本研究的目的是检查联苯美拉烷对从胎鼠获得的培养皮层神经元中谷氨酸细胞毒性的神经保护作用。短暂接触谷氨酸会显着降低细胞活力。在接触谷氨酸之前，将培养物暴露于浓度为 1-10 microM 的比芬美兰 24 小时，可降低谷氨酸的细胞毒性。相反，在未经预处理的情况下向含谷氨酸盐的培养基中添加联苯美拉恩不会影响谷氨酸盐的细胞毒性。 Bifemelane 不会影响 N-甲基-D-天冬氨酸 (NMDA) 诱导的电流，但较高浓度 (100 µM) 的药物会降低电流。这些发现表明，bifemelane 可防止谷氨酸神经毒性，而不影响 NMDA 受体。
This study was performed to examine the neuroprotective action of bifemelane against glutamate cytotoxicity in cultured cortical neurons obtained from fetal rats. Cell viability was markedly reduced by a brief exposure to glutamate. Glutamate cytotoxicity was reduced by exposing cultures to bifemelane at concentrations of 1-10 microM for 24 hr prior to glutamate exposure. In contrast, glutamate cytotoxicity was not affected by adding bifemelane to the glutamate-containing-medium without pretreatment. Bifemelane did not affect N-methyl-D-aspartate (NMDA)-induced currents, although the higher concentration (100 microM) of the drug reduced them. These findings suggest that bifemelane protects against glutamate neurotoxicity without affecting NMDA receptors.