论文部分内容阅读
目的:建立颞叶癫痫模型,探讨不同脑区给予多巴胺D1受体拮抗剂SCH23390对红藻氨酸所致的颞叶癫痫的影响。方法:实验于2004-08/12在解放军第一军医大学珠江医院全军神经医学研究所进行。①分组:取SD大鼠30只,随机分为生理盐水组3只,红藻氨酸组3只和实验组24只,实验组又分为海马、纹状体、黑质注射组各5只(共15只),以及同部位生理盐水注射作为对照,每组3只(共9只)。②造模:红藻氨酸组及实验组大鼠给红藻氨酸酸5μg(2.5g/L)右侧脑室注射制备颞叶癫痫模型,生理盐水组同部位给生理盐水2μL。③给药:实验组中的海马、纹状体、黑质注射组在相应部位缓慢注入1g/L的SCH233901μL,各部位以相同剂量生理盐水注入作为对照。④观察指标:观察各组间的大鼠行为变化及脑电图变化。3d后取脑作海马部TUNEL染色,观察海马部神经细胞凋亡情况。结果:30只大鼠全部进入结果分析。①行为变化:生理盐水组无癫痫发作。红藻氨酸组大鼠均出现癫痫发作,发作于脑室注射红藻氨酸后10min开始,1h达高峰。②脑电图变化:生理盐水组无尖波、棘波、棘慢综合波等痫性电活动表现,红藻氨酸组于注射后10min即有痫性波出现,其波幅为中幅及高幅波,但出现频率较低;1h左右癫痫发作达高峰时其波幅大部为高幅波,出现频率高;3~6h后波幅降低,12h后无痫性波出现。实验组中纹状体注射组波幅降低明显,与红藻氨酸组相比差异显著;黑质注射组亦有下降,而海马注射组无明显下降,与红藻氨酸组相比无差异。③细胞的凋亡:癫痫发作后伴随有海马细胞的凋亡,3d时明显。各脑区给予SCH23390后,海马部细胞凋亡减轻不一致,纹状体注射组阳性细胞数最少,与红藻氨酸组相比其差值有统计学意义(P﹤0.01)。结论:①一侧侧脑室注入红藻氨酸可成功建立癫痫模型。②红藻氨酸致痫后伴有海马神经凋亡改变,给予多巴胺D1受体拮抗剂SCH23390后,海马神经元凋亡减轻。③不同部位注射产生的凋亡细胞数不同,其中以纹状体注射所产生的凋亡细胞数最少,提示各部位在红藻氨酸所致的颞叶癫痫中的作用不同。
Objective: To establish a model of temporal lobe epilepsy to investigate the effect of dopamine D1 receptor antagonist SCH23390 on temporal lobe epilepsy induced by kainic acid in different brain regions. METHODS: The experiment was performed at the Institute of Neurology and Neurology, Zhujiang Hospital, First Military Medical University, People’s Liberation Army from August to December 12, 2004. Grouping: Thirty SD rats were randomly divided into three groups: saline group, kainic acid group and experimental group, the experimental group was divided into hippocampus, striatum and substantia nigra injection group (A total of 15), and the same site saline injection as a control, each group of 3 (a total of 9). (2) Modeling: Kainic acid group and experimental group rats were given temporal lobe epilepsy model by injection of kainic acid 5μg (2.5g / L) into the right ventricle. Normal saline group was injected with 2μL normal saline. ③ Administration: hippocampus, striatum and substantia nigra injection group in the experimental group were injected slowly with 1 g / L SCH233901 μL in the corresponding sites, and all the sites were injected with the same dose of saline as the control. ④Observation: The changes of behavior and EEG of rats in each group were observed. The brain was taken for TUNEL staining of hippocampus after 3 days to observe the neuronal apoptosis in the hippocampus. Results: All 30 rats entered the result analysis. ① behavior changes: saline-free seizures. The rats in kainic acid group all had seizures. The onset of seizures began at 10 min after injection of kainic acid in the ventricles and peaked at 1 h. ② EEG changes: There was no sharp wave, spike wave and spike-slow combination wave in the saline group, and the epileptic wave appeared in the kainic acid group 10 minutes after the injection, with amplitude of medium amplitude and high amplitude Amplitude wave, but the frequency of occurrence was lower. When the peak value of epileptic seizure peaked at 1h, most of the wave amplitude was high-amplitude wave with high frequency of occurrence. The amplitude was decreased after 3 ~ 6h and no epileptic wave appeared after 12h. In the experimental group, the amplitude of striatum injection decreased significantly, which was significantly different from that of kainic acid injection group. The substantia nigra injection group also decreased, while the hippocampal injection group did not significantly decline, no difference compared with kainic acid group. ③ cell apoptosis: accompanied by apoptosis of hippocampal cells after seizure, 3d obvious. After administration of SCH23390 in various brain regions, the apoptosis of hippocampus cells was inconsistent and the number of positive cells in striatum injection group was the lowest. Compared with kainic acid group, the difference was statistically significant (P <0.01). Conclusion: ① One side of the lateral ventricle into kainic acid can be successfully established epilepsy model. ② After kainic acid-induced seizures, apoptosis of hippocampal neurons was changed. After dopamine D1 receptor antagonist SCH23390 was given, apoptosis of hippocampal neurons was relieved. ③ different parts of the injection of apoptotic cells produced by different number of apoptotic cells injected into the striatum produced the least, suggesting that all parts of the kainic acid-induced temporal lobe epilepsy in different roles.