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目的观察大麻素anandam ide(AEA)对大鼠海马脑片突触传递长时程增强效应(LTP)及其对海马细胞凋亡的影响。方法选用W istar大鼠,迅速断头取脑,剥离海马,制作厚约400μm的脑片,运用电生理的方法观察AEA及其CB1受体拮抗剂AM251对海马脑片CA1区LTP的影响,并采用AO/EB双荧光染色,激光共聚焦显微镜观察AEA和AM251对原代培养大鼠海马神经元凋亡的形态学改变,流式细胞仪技术观察AEA和AM251对原代培养大鼠海马神经元凋亡率的影响。结果AEA明显抑制大鼠海马脑片LTP的产生,同时AEA有促进原代培养大鼠海马神经元凋亡的作用,而AM251可逆转AEA的上述作用。结论AEA对大鼠海马脑片CA1区LTP有抑制作用,并且AEA有促使神经元凋亡的神经毒性作用。
Objective To observe the effect of cannabinoid anandam ide (AEA) on the synaptic transmission of long-term potentiation (LTP) and its effect on hippocampal apoptosis in hippocampal slices of rats. Methods Wistar rat was used to rapidly decapitate the brain and dissect the hippocampus to make slices with a thickness of 400μm. The electrophysiologic method was used to observe the effects of AEA and its CB1 receptor antagonist AM251 on the LTP in CA1 region of hippocampal slices. The morphological changes of hippocampal neurons of primary cultured AEA and AM251 were observed by AO / EB double staining and confocal laser scanning microscope. Flow cytometry was used to observe the effect of AEA and AM251 on primary cultured rat hippocampal neurons Effect of apoptosis rate. Results AEA significantly inhibited the LTP production in rat hippocampal slices, while AEA promoted the primary cultured rat hippocampal neurons apoptosis, while AM251 reversed the effect of AEA. Conclusion AEA can inhibit the LTP of CA1 area in rat hippocampal slices, and AEA can induce neuronal apoptosis.