Jørgensen M B, Diemer N H
Acta Neurol Scand. 1982 Nov;66(5):536-46. doi: 10.1111/j.1600-0404.1982.tb03140.x.
Male Wistar rats were subjected to 20 min of cerebral ischemia by means of 4-vessel occlusion. The topography of regional, selective neuron loss in this model corresponded to areas with pronounced glutamate high affinity uptake (presynaptic receptors), suggesting that transmitter glutamate is involved in the mechanism of neuron damage. One group of animals was injected with the glutamate antagonist, glutamic acid diethyl ester (GDEE) before ischemia. The regional neuron loss was rated using a semiquantitative scale. No statistically significant difference was found between the groups. The results do not exclude a possible role of transmitter glutamate in the pathogenesis of ischemic brain damage. More specific and potent glutamate antagonists are needed in order to clarify such a mechanism.
雄性Wistar大鼠通过四血管闭塞法遭受20分钟的脑缺血。该模型中局部、选择性神经元损失的地形分布与谷氨酸高亲和力摄取(突触前受体)明显的区域相对应,这表明递质谷氨酸参与了神经元损伤机制。一组动物在缺血前注射了谷氨酸拮抗剂二乙谷氨酸酯(GDEE)。使用半定量量表对局部神经元损失进行评分。两组之间未发现统计学上的显著差异。这些结果并不排除递质谷氨酸在缺血性脑损伤发病机制中的可能作用。为了阐明这种机制,需要更特异和有效的谷氨酸拮抗剂。