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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 investigate the expression of GAP-43 and brain-derived neurotrophic factor (BDNF) receptor TrkB in hippocampus of pilocarpine-induced rat hippocampus and its significance. Methods The in situ hybridization histochemical method was used to study the changes of GAP-43 and TrkB mRNA expression in the hippocampus of rats induced by pilocarpine (PILO). RESULTS: TrkB mRNA expression in hippocampal dentate gyrus granule cells, CA 3 area and CA 1 pyramidal cell layer was significantly higher than that in control group (P <0.01 or 0.05) 3 to 6 hours after pilocarpine-induced status epilepticus. The first 7 to 30 days, showing the second enhanced expression. After 6 ~ 12hours after operation, the expression of GAP-43 mRNA in hippocampus granulosa cells of rats that did not express GAP-43 under normal conditions was significantly higher than that of the control group (P <0.01), decreased from 24 hours to 7 days, Chronic phase expression again higher than the control group. Conclusion GAP-43 and TrkB are the pathological basis of temporal lobe epilepsy - the important molecular mechanism of germination of mossy fiber in hippocampus. The effect of BDNF on mossy fiber is partly through GAP-43.