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李红斌, 韩会丽, 马文裴, 董志芳, 徐 林. 2007: “不完全氧糖剥夺”对A型氨基丁酸受体介导的抑制性突触后膜电流的增强作用. 动物学研究, 28(5): 491-496.
引用本文: 李红斌, 韩会丽, 马文裴, 董志芳, 徐 林. 2007: “不完全氧糖剥夺”对A型氨基丁酸受体介导的抑制性突触后膜电流的增强作用. 动物学研究, 28(5): 491-496.
LI Hong-bin, HAN Hui-li, MA Wen-pei, DONG Zhi-fang, XU Lin. 2007. Enhancement of GABAA Receptor-Mediated Inhibitory Postsynaptic Currents Induced by “Partial Oxygen-Glucose Deprivation”. Zoological Research, 28(5): 491-496.
Citation: LI Hong-bin, HAN Hui-li, MA Wen-pei, DONG Zhi-fang, XU Lin. 2007. Enhancement of GABAA Receptor-Mediated Inhibitory Postsynaptic Currents Induced by “Partial Oxygen-Glucose Deprivation”. Zoological Research, 28(5): 491-496.

“不完全氧糖剥夺”对A型氨基丁酸受体介导的抑制性突触后膜电流的增强作用

Enhancement of GABAA Receptor-Mediated Inhibitory Postsynaptic Currents Induced by “Partial Oxygen-Glucose Deprivation”

  • 摘要: 摘要: 氧糖剥夺模型作为研究脑缺血的离体模型被广泛使用,该模型模拟了局灶性脑缺血的病理变化。然而在缺血病灶中心区与正常脑组织之间的称为缺血半暗带的区域,脑血流也有程度不一的降低。为了模拟这种病理变化,我们发展了一种中等程度氧糖剥夺的离体脑片模型,该模型满足两个条件,氧气部分剥夺而葡萄糖完全剥夺。临床上通过增强A型γ-氨基丁酸受体介导的抑制活动可以阻止海马神经元的坏死,但其机制不清楚。因此我们采用全细胞膜片钳的记录方法,研究中等程度的氧糖剥夺对海马脑片CA1区神经元的A型γ-氨基丁酸受体介导的抑制性突触后膜电流(IPSCs)的影响。我们发现中等程度的氧糖剥夺使A型γ-氨基丁酸受体电流(IPSCs)的峰值增加而衰减时程延长。进一步研究发现该电流的峰值增加是由于A型γ-氨基丁酸受体-氯离子通道的电导增加所致,而与氯离子的反转电位无关。这些发现提示神经系统在中等程度脑缺血的早期阶段可以通过内稳态机制来维持兴奋性系统和抑制性系统之间的平衡。关键词: 中等程度脑缺血, A型γ-氨基丁酸受体, 抑制性突触后膜电位, 峰值

     

    Abstract: Abstract: Oxygen/glucose deprivation (OGD) has been widely used as an in vitro model of focal ischemia, where the blood flow is severely reduced and neurons rapidly die. However, adjacent to the focal region is ‘penumbra’, where residual blood flow remains oxygen and glucose supplies are at low levels. To model this pathological genesis, we developed a partial OGD (pOGD) protocol in a rat brain slice. This model met two requirements: oxygen was partially deprived and glucose was reduced in the perfusion buffer. Therefore we investigated the effect of pOGD on gama-aminobutyric acid (GABAA) receptor-mediated inhibitory postsynaptic currents (IPSCs) in CA1 neurons of a hippocampal slice through whole-cell patch-clamp technique. We found that the amplitude and decay time of IPSCs were increased immediately during pOGD treatment. And the enhancement of IPSCs amplitude resulted from an increase of the synaptic conductance without a significant change in the reversal potential of chloride. These results suggested that the nervous system could increase inhibitory neurotransmission to offset excitation by homeostasis mechanisms during the partial oxygen and glucose attack.

     

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