Effects of the AMPA-Receptor Antagonist, NBQX, on Neuron Loss in Dentate Hilus of the Hippocampal Formation after 8, 10, or 12 Min of Cerebral Ischemia in the Rat
Effects of the AMPA-Receptor Antagonist, NBQX, on Neuron Loss in Dentate Hilus of the Hippocampal Formation after 8, 10, or 12 Min of Cerebral Ischemia in the Rat
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DOI：
10.1097/00004647-199702000-00003
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发表时间：
1997-02
影响因子：
6.3
通讯作者：
P. Hu;N. Diemer;T. Bruhn;F. Johansen
中科院分区：
文献类型：
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作者：
P. Hu;N. Diemer;T. Bruhn;F. Johansen
α-氨基-3-羟基-5-甲基-4-异恶唑（AMPA）受体拮抗剂2，3-二羟基-6-硝基-7-氨磺酰基-苯并（F）喹喔啉（NBQX）对短暂脑缺血后海马CA 1区锥体细胞具有保护作用。脑缺血后海马结构齿状门区除CA 1区锥体细胞外，含生长抑素（SS）的神经元也消失。我们研究了NBQX的保护作用，在门SS神经元和海马CA 1锥体细胞后8，10，或12分钟的四血管闭塞缺血在全身性低血压。在诱导缺血或假手术后0、10和25天给予NBQX 3 × 30 mg/kg，所有大鼠均存活7天。NBQX对非缺血对照组大鼠肺门SS神经元和CA_1锥体细胞的数量和形态无影响。缺血8分钟后，NBQX防止了门SS神经元的丢失。缺血10和12分钟后，NBQX对齿状门SS神经元的丢失没有显着影响。然而，在所有的缺血组，NBQX显着减少损失的CA 1锥体细胞相比，对照组大鼠。随着缺血时间的延长，这种神经保护作用逐渐减弱。我们的研究结果支持了门区SS神经元是脑中最易缺血的神经元之一的观察。我们发现，以普遍接受的剂量给予NBQX可以保护门中快速死亡的SS神经元免于短暂的缺血发作。
The α-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) receptor antagonist, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX), offers protection to hippocampal CA1 pyramidal cells after short episodes of transient cerebral ischemia. Besides CA1 pyramidal cells, neurons containing somatostatin (SS) and located in the dentate hilus of the hippocampal formation are lost after cerebral ischemia. We studied the protective effects of NBQX on SS neurons in the hilus and on hippocampal CA1 pyramidal cells following 8, 10, or 12 min of four-vessel occlusion ischemia during systemic hypotension. NBQX was administered 3 × 30 mg/kg at 0, 10, and 25 after induction of ischemia or sham, and all rats survived for 7 days. NBQX given to control rats without ischemia had no influence on number or morphology of hilar SS neurons and CA1 pyramidal cells. After 8 min of ischemia, NBQX prevented loss of hilar SS neurons. After 10 and 12 min of ischemia, NBQX had no significant effects on loss of SS neurons in the dentate hilus. However, in all ischemic groups, NBQX significantly reduced loss of CA1 pyramidal cells as compared to control rats. This neuroprotective effect decreased gradually and significantly as the time of ischemia increased. Our results support the observation that SS neurons in hilus are among the most ischemia-vulnerable neurons in the brain. We found that administration of NBQX in generally accepted dosages can protect the rapidly dying SS neurons in hilus from only brief episodes of ischemia.