目的：观察杏仁核点燃癫痫大鼠BKCa通道β4亚基动态演变情况。方法：建立杏仁核点燃癫痫大鼠 模型，随机分对照组、点燃24 h组、30 d组、60 d组。采用尼氏染色观察各组神经元损伤情况；采用实时定 量PCR、蛋白质印迹、免疫组织化学检测发作后24 h、30 d、60 d大鼠脑内BKCa通道β4亚基表达的动态改 变情况。结果：相比对照组，杏仁核点燃癫痫模型大鼠皮质及海马CA1、CA3区神经元均有明显缺失，且随 着点燃时间增加，神经元计数呈下降趋势，各组差异有统计学意义（P＜0.05）。点燃后24 h，皮质及海马 BKCa通道β4亚基表达下降，且随着点燃时间增加呈下降趋势，差异有统计学意义（P＜0.05）。结论：杏仁 核点燃可导致脑内神经元持续损伤，同时伴随相应部位BKCa通道β4亚基表达下降，推测β4亚基可能参与 了杏仁核点燃癫痫模型发生发展的过程。

To determine the dynamic changes of BKCa channel β4 subunit in amygdala kindled epilepsy rat model. Methods: The animals were divided into control group, 24-hour group, 30-day group and 60-day group. Epilepsy rats were kindled by amygdala nuclear stimulation. The injury of neurons in each group was detected by Nissl’s staining. Real-time quantitative PCR, western blot and immunohistochemistry were used to detect the dynamic changes of BKCa channel β4 subunit expression in the brain of rats 24 hours, 30 days and 60 days after being kindled. Results: Compared with the control group, the neurons in CA1 and CA3 regions of the hippocampus and cortex of rats in the amygdala kindled epilepsy model were significantly lost, and the number of neurons showed a decreasing trend with the increase of the kindling time (P<0.05). The expression of β4 subunit of BKCa channel in cortex and hippocampus decreased 24 hours after being kindled, and showed a downward trend with the increase of kindling time (P<0.05). Conclusion: The results suggested that amygdala kindling can cause the persistent damage of neurons which accompanied by the decrease of β4 subunit expression. It is speculated that β4 subunit may be involved in the development of amygdala kindled epilepsy rat model.