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神经细胞缺血缺氧后突触后电流的频率或幅度出现变化 ,提示氨基酸类神经递质释放的变化。急性缺血缺氧时 ,自发性兴奋性突触后电流和抑制性突触后电流均受到抑制 ,诱发性兴奋性突触后电流幅度增高。长期慢性缺氧情况下 ,NMDA受体介导的兴奋性突触后电流受到抑制。缺氧预适应后 ,γ 氨基丁酸释放增加 ,谷氨酸释放减少。多次重复急性缺氧抑制诱发性兴奋性突触后电流的幅度 ,说明长期慢性缺氧及缺氧预适应启动神经细胞的保护机制。腺苷通过调节氨基酸递质的释放 ,对神经细胞具有明显的保护作用 ,但对于缺血缺氧所造成的损伤却未见修复作用。
Changes in the frequency or amplitude of postsynaptic currents after ischemia and hypoxia in nerve cells suggest changes in the release of amino acid neurotransmitters. Acute hypoxia and hypoxia, spontaneous excitatory postsynaptic currents and inhibitory postsynaptic currents are inhibited, induced excitatory postsynaptic currents increased. Under long-term chronic hypoxia, NMDA receptor-mediated excitatory postsynaptic currents are inhibited. After hypoxic preconditioning, γ-aminobutyric acid release increased, glutamate release decreased. Repeatedly repeated acute hypoxia inhibited the amplitude of induced excitatory postsynaptic currents, suggesting that long-term chronic hypoxia and hypoxia preconditioning activate neuroprotective mechanisms. Adenosine has a significant protective effect on nerve cells by regulating the release of amino acid neurotransmitter, but no effect is found on the damage caused by ischemia and hypoxia.