Objective: To investigate mitochondrial damage in hippocampal neurons in adenosine Al receptor knock-out mice after pentetrazole (PTZ) kindling. Methods: The adenosine Al receptor knock-out (KO) mice (n = 30) and wild type (WT) mice (n = 30) were randomly divided into control group and 6 h, 24 h, 7 d and 30 d post-epilepsy groups (n = 5 respectively). Kindling model of epilepsy was induced by intraperitoneal injection of PTZ. Flow cytometry was used to detect mitochondria membrane potentials and immunofluorescence was applied to measure cytochrome C activity. Results: Compared with those in the control group, the mitochondria membrane potentials were significantly lower and the cytochrome C activity was higher in all the post-epilepsy groups (P<0. 05), both in KO mice and WT mice. Compared with those in the WT mice, the mitochondria membrane potentials were lower and the cytochrome C activity was higher in all the KO mice after epilepsy (P<0. 05). Conclusion: The mitochondrial damage is evident in hippocampal neurons at early stage of epilepsy. Al adenosine receptor activation could attenuate this kind of mitochondrial damage in mice after epilepsy. The mitochondrial damage is evident in hippocampal neurons at early stage of epilepsy. Al adenosine receptor activation could attenuate this kind of mitochondrial damage in mice after epilepsy.%目的:观察腺苷A1受体基因敲除小鼠戊四氮致痫后海马神经细胞线粒体功能的损伤.方法:腺苷A1受体基因敲除小鼠和野生型小鼠各30只,各随机分为对照组、致痫后6h、24 h、7d、30 d组,每组6只；戊四氮点燃制作癫痫模型；于各时间点取小鼠海马,流式细胞仪测线粒体膜电位,免疫荧光测细胞色素C(cyt C)的表达.结果:基因敲除小鼠和野生型小鼠致痫后6h、24 h、7d及30 d组的线粒体膜电位均低于对照组(P＜0.05),cyt C释放量均高于对照组(P＜0.05)；除对照组外,基因敲除小鼠致痫后6h、24 h、7d及30 d组的线粒体膜电位均低于野生型小鼠(P＜0.05),cyt C释放量均高于野生型小鼠(P＜0.05).结论:癫痫早期即可出现海马线粒体功能损伤,腺苷A1受体有助于减轻癫痫小鼠海马线粒体损伤.
展开▼
