摘要
目的了解热性惊厥导致神经损伤的详细机制,以筛选更有效的治疗药物。方法选取出生10 d的新生雄性Wistar大鼠建立热性惊厥模型。通过大鼠脑片灌流和全细胞记录的膜片钳技术检测了热性惊厥时海马齿状回颗粒细胞3种谷氨酸受体的兴奋性突触后电流(EPSC):分别由NMDA和AMPA受体介导的EPSC和混合EPSC。并与正常对照组大鼠进行比较。结果对照组大鼠齿状回的混合EPSC为(138±23)pA,而热性惊厥组混合EPSC为(186±29)pA,较前者明显上升(P<0.05)。同时发现热性惊厥组齿状回由NMDA受体介导的EPSC也较对照组明显升高,两者分别为(92±14)pA和(60±10)pA(P<0.05)。但由AMPA受体介导的EPSC热性惊厥组与对照组相比无明显改变,两者分别为(65±17)pA和(68±11)pA(P>0.05)。结论热性惊厥选择性使齿状回NMDA受体兴奋性增加,但不影响AMPA功能,这构成了热性惊厥神经损伤的一个重要环节。
Objective To investigate the mechanism of febrile seizure-induced brain damage,and screen out the medication.Methods Brain slices were superfused and whole cell recording patch clamp technique was carried out at granule cells to investigate three kinds of excitatory postsynaptic currents（EPSC）in rat dentate gyrus：NMDA and AMPA receptor-mediated EPSC,and mixed EPSC.Results The mixed EPSC in febrile seizure group[（186±29） pA]was significantly higher than in control group[（138±23） pA]（P0.05）.NMDA-mediated EPSC was increased in febrile seizure group[（92±14）pA]as compared with control group[（60±10）pA]（P0.05）.On the contrast,AMPA-mediated EPSC showed no significant difference between two groups[EPSC in control group and febrile group was（68±11） and（65±17） pA respectively].Conclusion Febrile seizure caused a glutamate receptor selective excitability in dentate gyrus.NMDA-mediated EPSC was increased and AMPA-mediated EPSC seemed silent at the present experimental condition.The finding revealed an important point of the mechanism of febrile seizure.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2011年第2期156-159,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
国家自然科学基金资助项目(No.30872796)
关键词
热性惊厥
海马
谷氨酸受体
兴奋性突触后电流
febrile seizure
hippocampus
glutamate receptor
excitatory postsynaptic currents
