Down-regulateon of glutamate receptor 2 mRNA could lead to formation of GluR2-lacking, Ca2+-permeable AMPA receptors and increased toxicity of endogenous glutamate, which may be involved in the mechanisms of thedelayed neuronal death.

• 结论 我们的研究显示，成年大鼠癫痫持续状态后海马神经元发生的是选择性的、迟发性的损伤，而AMPA受体的亚单位谷氨酸受体-2的下调形成了Ca~(2+)渗透性的AMPA受体，增加了内源性谷氨酸的兴奋毒性，可能参与了迟发性神经元损伤的机制。