摘要
目的探讨EP2在小鼠海马齿状回突触传递中的作用及其机制。方法细胞外记录技术记录海马脑片穿通纤维-齿状回颗粒细胞突触的场兴奋性突触后电位（fEPSP）。结果①EP2的激动剂Butaprost增强海马齿状回突触传递和降低双脉冲比（paired-pulse ratio,PPR）,此效应被EP2的拮抗剂AH6809所阻断。②Forskolin单独或Forskolin＋AH6809均可增强fEPSP的斜率。③EP2增强突触效能的效应由PKA,ERK和IP3途径介导。结论多信号转导途径可能参与EP2激活诱导的突触传递增强。
Objective To evaluate the role of EP2 in synaptic transmission in dentate gyrus of hippocampus. Methods Field excitatory post-synaptic potentials （fEPSP） were recorded at the perforated path-granule neurons in dentate gyrus in vitro. Results （1） Butaprost, an agonist of EP2, enhanced the synaptic transmission in dentate gyrus and decreased the paired-pulse ratio, and these effects were reversed by bath application of AH6809 （EP2 antagonist）. （2） Application of Forskolin alone or with AH6809 elevated the slope of fEPSP. （3） The Butaprostinduced responses were mediated via PKA, ERK and IP3 signal pathways. Conclusion Multiple signal pathways were involved in the EP2 activation-mediated enhancement of synaptic transmission.
出处
《西安交通大学学报（医学版）》
CAS
CSCD
北大核心
2010年第1期59-62,共4页
Journal of Xi’an Jiaotong University（Medical Sciences）
基金
湖北省卫生厅基金资助项目（No.JX2877）
湖北省教育厅基金资助项目（No.Q200613002）.
