出 处:《中华神经科杂志》2009年第7期463-467,共5页Chinese Journal of Neurology
基 金:卫生部部属医院临床学科重点资助项目(2007-353);湖南省科技厅科技计划资助项目(2007TP4005)
摘 要:目的探讨表达生长抑素(SS)的中间神经元在颞叶癫癎的发生和自我修复中的作用。方法建立匹罗卡品致疴大鼠模型。免疫组织化学方法检测各时间点海马不同区域SS中间神经元的数目变化及其轴突出芽情况;结合Fluoro—Jade B(FJB)行免疫荧光双标方法特异性检测大鼠癫癎持续状态(status epilepticus,SE)后7d和60d海马不同区域ss中间神经元及其轴、树突的变性情况。结果实验组大鼠海马各区SS阳性神经元数目均在SE后7d减至最低(门区11.1±3.3,CA,区2.8±0.9,CA3区1.8±0.7,t=13.519、9.644、8.808,均P〈0.01),慢性期开始部分恢复,sE后60d时CA1区ss神经元数目(12.8±1.5)超过对照组(8.8±1.3,t=-4.506,P〈0.01),但门区和CA,区SS神经元数目(分别为25.5±4.6和4.8±0.8)仍明显低于正常水平(t=4.691、3.953,P〈0.01);sE后30d大鼠海马回腔隙-分子层(lacunosum—moleculare,lm)和齿状回外分子层出现大量SS染色阳性纤维,60d时海马CA1区全层均可见大量增多的SS阳性纤维。实验组中SE后7d的海马CA1区、60d的CA1、CA3区和门区均可观察到少部分被FJB染色的SS中间神经元胞体及其轴、树突。结论SS中间神经元的缺失在颞叶癫癎的发生中起重要作用,其缺失部分是由于神经元的变性死亡所致;慢性期CA1区SS阳性纤维大量增多,可能在颞叶癫癎的发生和自我修复中起重要作用。Objective To investigate the roles of somatostatin (SS) positive interneurons in the development and compensation of temporal lobe epilepsy. Methods Pilocarpine-induced epilepsy rat model was established. Immunohistochemistry method was used to detect number changes and axonal sprouting of SS positive interneurons in different domains of the hippocampus at different time points.Degeneration of SS positive interneurons and their neurophils were detected by the double immunofluoreseence staining with SS and Fluoro-Jade B ( FJB ) at 7 and 60 days after status epilepticus (SE). Results In the experimental rat group, the number of SS positive neurons deereased in each hippoeampal domain, and it reached the lowest at 7 days post-SE (There were 11.1 ± 3.3 in hilus, 2. 8 ± 0. 9 in CA1 region and 1.8 ±0. 7 in CA3 region, t = 13. 519, 9. 644 and 8. 808, all P 〈0. 01 ). In chronic phase, the number of SS neurons gradually recovered, and exceeded the control group in CA1 area at 60 days post-SE (12.8 ± 1.5 vs 8.8 ± 1.3, t = -4. 506, P 〈0. 01 ) , however, the number of SS neurons in the hilus (25.5 ± 4. 6) and CA3 area (4. 8 ± 0. 8 ) remained significantly less than normal levels (t value were 4. 691 and 3. 953, both P 〈 0. O1 ). Increased SS positive fibers were found in the lacunosum-molecular (lm) layer and outer molecular layer of dentate gyrus after 30 days post-SE, and numerous SS positive fibers were seen throughout the layers of area CA1 at 60 days post-SE. Double immunofluoreseenee revealed that a few SS positive interneurons and fibers were also labeled by FJB in area CA1 at 7 days post-SE and in CA domain/hilus at 60 days post-SE. Conclusions SS interneurons loss plays an important role in the development of temporal lobe epilepsy. The loss is partially caused by the degeneration and death of neurons; SS positive neurophils increase within area CA1 in chronic phase may play a significant role in the generation and compensation of temporal lobe epilepsy.
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