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氯胺酮可保护培养的新皮质神经元免受缺氧损伤。

Ketamine protects cultured neocortical neurons from hypoxic injury.

作者信息

Weiss J, Goldberg M P, Choi D W

出版信息

Brain Res. 1986 Aug 13;380(1):186-90. doi: 10.1016/0006-8993(86)91447-2.

DOI:10.1016/0006-8993(86)91447-2
PMID:3756469
Abstract

The general anesthetic ketamine, which has recently been reported to block the excitation of cortical neurons by N-methyl-D-aspartate (NMDA), was found to markedly reduce neuronal loss in murine neocortical cell cultures exposed to a hypoxic atmosphere or to cyanide. These observations may be relevant to attempts to find pharmacological means of minimizing hypoxic brain damage in the clinical setting.

摘要

据最近报道,全身麻醉剂氯胺酮可阻断N-甲基-D-天冬氨酸(NMDA)对皮质神经元的兴奋作用,研究发现,在暴露于低氧环境或氰化物的小鼠新皮质细胞培养物中,氯胺酮能显著减少神经元损失。这些观察结果可能与在临床环境中寻找将缺氧性脑损伤降至最低的药理学方法的尝试相关。

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Ketamine influences CLOCK:BMAL1 function leading to altered circadian gene expression.氯胺酮影响时钟:BMAL1 功能,导致昼夜节律基因表达改变。
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