发育中的海马神经元缺氧后N-甲基-D-门冬氨酸受体通道电流变化及腺苷干预作用

目的研究缺氧对发育中的海马神经元N-甲基-D门冬氨酸（NMDA）受体通道电流的影响及腺苷干预作用的离子通道机制。方法应用膜片箝技术分别对培养日龄为6、16d的海马神经元缺氧前、后NMDA受体通道电流进行全细胞记录，测定其电流的最大幅值并研究腺苷对其干预作用。结果在缺氧状态下，培养日龄为6d的海马神经元，其NMDA受体通道电流最大幅值与正常对照组相比显著升高（P〈0．05）。培养日龄为16d的海马神经元，其NMDA受体通道电流最大幅值与正常对照组相比亦显著升高（P〈0．001）。予腺苷干预则使缺氧状态下培养日龄为6d的海马神经元NMDA受体通道电流最大幅值显著降低（P〈0．01）。而培养日龄为16d的海马神经元，腺苷干预后其NMDA受体通道电流最大幅值无明显变化。绪论缺氧使海马神经元NMDA受体通道电流幅值升高。腺苷通过降低NMDA受体通道电流幅值，对来成熟的海马神经元缺氧性损伤有一定的保护作用。

Changes of N-Methyl-D-Aspartate-Receptor-Channels Current in Developing Hippocampal Neurons after Hypoxia and Effect of Adenosine Intervention

Objective To study the changes of N-methyl-D-aspartate(NMDA)-receptor-channels current in developing hippocampal neurones during hypoxia and effect of adenosine intervention.Methods Whole-cell patch-clamp techniques cultured hippocampal neurons whose cultured day were 6 days and 16 days respectively,the amplitude of the NMDA-receptor-channels currents of hippocampal neuron were determined.And the effect of hypoxia on the NMDA-receptor-channels current,and adenosine regulatory mechanisms in cultured hippocampal neurons were explored.Results During hypoxia,compared with control group,the amplitude of the NMDA-receptorchannels currents of hippocampal neuron whose cultured day was 6 days were significantly increased(P<0.05).Moreover,the amplitude of the NMDA-receptor-channels currents of hippocampal neuron whose cultured day was 16 days were also significantly increased(P<0.001).During hypoxia,adenosine could significantly decrease the amplitude of the NMDA-receptor-channels currents of hippocampal neuron whose cultured day was 6 days,whereas,the amplitude of the NMDA-receptor-channels current of hippocampal neuron whose cultured day was 16 days was not decreased obviously by adenosine.Conclusions The results suggest that NMDA-receptor-channels in rat hippocampal neurons are activated significantly during hypoxia.During hypoxia,the NMDA-receptor-channels current of immatured hippocampal neuron is decreased obviously by adenosine,which may be related to the suppress of adenosine to the increase of calcium in cells.