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作 者:李国良[1] 肖波[1] 谢光洁[1] 章蓓[1] 李昌奇 伍校琼
机构地区:[1]中南大学湘雅医院神经内科,长沙410008 [2]湘雅医学院神经生物学教研室
出 处:《临床神经病学杂志》2003年第3期150-152,共3页Journal of Clinical Neurology
基 金:教育部高等学校优秀青年教师教学科研奖励计划基金(2001-182)
摘 要:目的 探讨生长相关蛋白(GAP-43)和脑源性神经营养因子(BDNF)受体TrkB基因在匹罗卡品致癎大鼠海马的表达及其意义。方法 应用原位杂交组织化学方法研究匹罗卡品(PILO)致癎大鼠海马GAP-43及TrkB mRNA表达的变化。结果 匹罗卡品致癫癎持续状态后3~6小时,海马齿状回颗粒细胞、CA_3区及CA_1区锥体细胞层TrkB mRNA表达显著高于对照组(P<0.01或0.05);在慢性期第7~30天,呈现第2次表达增强。致癎后6~12小时,正常状态下并不表达GAP-43的大鼠海马颗粒细胞其GAP-43 mRNA表达较对照组显著增高(P<0.01),24小时~7天表达减少,在癫癎慢性期表达再次高于对照组。结论 GAP-43及TrkB是颞叶癫癎病理基础——海马苔藓纤维出芽的重要分子机制;BDNF对苔鲜纤维的作用部分是通过GAP-43实现的。Objective To explore the expression and its significance of growth-associated protein(GAP-43 ) and brain-derived neurotrophic factor (BDNK) receptor TrkB gene in rat hippocampus after epilepsy induced by pilocarpine (PILO). Methods In situ hybrid histochemical method was used to observe the changes of the expression of GAP-43 and TrkB mRNA in hippocampus after status epilepticus( SE) induced by PIOL. Results At 3 - 6h following the onset of status epilepticus(SE), TrkB mRNA expression was dramatically high than control groups in the dentate gyrus granule cell and CA3,CA1 pyramidal cell layers(P <0.01 or 0.05)and also demonstrated a second peak during chronic period 7 - 30 days after PILO-induced SE. At 6- 12h after SE,GAP-43 mRNA levels increased obviously than control groups in granule cells which normally do not express GAP-43 mRNA ( P < 0.01) , then attenuated after 24h - 7day, but again elevated above control levels during chronic period of epilepsy. Conclusion Changes of TrkB and GAP-43 mRNA levels were important molecul mechanisms of hippocampal mossy fiber sprouting underlying epileptogensis. Influence of BDNF on mossy fiber sprouting might partly act via GAP-43 at least.
关 键 词:匹罗卡品 大鼠 颞叶癫痫 生长相关蛋白 脑源性神经营养因子
分 类 号:R742.1[医药卫生—神经病学与精神病学]
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