新生大鼠缺氧缺血脑损伤（HIBD）中显著增加的自噬表达可导致海马锥体神经元细胞的死亡增加，影响远期学习记忆能力。研究者在前期研究中发现：在发育期大鼠反复惊厥模型中，Ca2+通透性AMPA/红藻氨酸通道（Ca-A/K通道）在Zn2+介导神经兴奋毒性损伤的信号传导通路中起着重要作用。提示我们Ca-A/K通道可能同样参与缺氧缺血的应激损伤过程。本实验拟在体外细胞培养以及整体新生大鼠缺氧缺血脑损伤模型中应用分子生物学、形态学及功能检测技术，观察新生期缺氧缺血后海马各亚区的Ca-A/K基因表达变化，以及与cathepsin B、自噬/凋亡标记分子LC-3和认知功能损害的关系,以期阐明在HIBD中，Ca-A/K通道介导的神经元损伤具有自噬特征，其生化机制可能涉及组织蛋白酶途径，而早期进行合理的干预，可能减轻神经系统远期功能障碍。

The high induction of autophagy in rat hippocampal pyramidal neurons after hypoxic-ischemic brain damage（HIBD） has been confirmed to significantly increase the death of neurons, and affect the further capacity of learning and memorization. In our previous study, we found that the Ca2+ permeable AMPA/Kainate channels (Ca-A/K channels) play an important part in injury of unbalanced Zn2+ flux in the rat model of recurrent neonatal seizure,which suggests us that Ca-A/K channels may also play an important role in damage of rat hippocampal pyramidal neurons after HIBD. The current study aims to determine the change of Ca-A/K gene expression in the pyramidal neurons in individual hippocampal sections following neonatal hypoxia-ischemia, to reveal their links with the cathepsin B and LC-3 by biological, morphological and functional investigations in in vitro cells as well as whole animal models of hypoxia-ischemia, and to determine the damage in rat hippocampal pyramidal neurons after HIBD mediated by Ca-A/K channel is a typical autophagic death, which mechanism invovling in the cathepsins, and early interventions to the autophagic mechanism may attenuate the injury of hippocampal neurons.