PROTECTION AGAINST ISCHEMIC HIPPOCAMPAL CA1 DAMAGE IN THE RAT WITH A NEW NON-NMDA ANTAGONIST, NBQX
PROTECTION AGAINST ISCHEMIC HIPPOCAMPAL CA1 DAMAGE IN THE RAT WITH A NEW NON-NMDA ANTAGONIST, NBQX
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DOI：
10.1111/j.1600-0404.1992.tb08052.x
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发表时间：
1992-07-01
影响因子：
3.5
通讯作者：
HONORE, T
中科院分区：
文献类型：
--
作者：
DIEMER, NH;JORGENSEN, MB;HONORE, T
两种谷氨酸拮抗剂在大鼠完全短暂性脑缺血模型中进行了测试。缺血10min后6d，海马CA1区锥体神经元平均损失率为73%。给予AMPA(α-氨基-3-羟基-5-甲基-4-异恶唑)拮抗剂NBQX(2，3-dihydro-6-nitro-7-sulfamoyl-benzo(F)quinoxaline)可使缺血前、缺血后即刻和缺血后1h的锥体神经元损失率分别减少1%、11%和15%。竞争性NMDA拮抗剂MK-801(地佐西平)对该模型无保护作用。我们认为，AMPA受体的转导机制是由缺血致敏的，而NBQX阻断缺血后对CA1细胞的主要谷氨酸能输入，削弱了“正常”的缺血后兴奋性传递的有害作用。
Two glutamate antagonists were tested in a rat model of complete, transient cerebral ischemia. Six days after 10 min ischemia the mean loss of hippocampal CA1 pyramidal neurones was 73%. Administration of the AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid) antagonist NBQX (2,3-dihydro-6-nitro-7-sulfamoyl-benzo(F)quinoxaline) reduced the pyramidal neurone loss to 1%, 11% and 15%, when given before, immediately after or 1 h after ischemia, respectively. MK-801 (dizocilpine), a competitive NMDA antagonist gave no protection in this model. We suggest that the AMPA receptor transduction mechanisms are sensitized by ischemia and that the postischemic blockade of the main glutamatergic input to the CA1 cells with NBQX impairs the deleterious effect of "normal" postischemic excitatory transmission.