目的：研究p42/44 MAPK通路在烟碱诱导大鼠海马CA1区长时程增强(LTP)形成中的作用.方法：细rnrn胞外场电位记录离体海马脑片CA1区锥体细胞层群体峰电位；蛋白质印迹检测p42/44 MAPK磷酸化程度及其总蛋白表达.结果：PD98059 25 μmol/L和50 μmol/L呈剂量依赖性抑制烟碱(10 μmol/L)诱导大鼠海马CA1区LTP的形成；在烟碱诱导LTP形成的海马CA1区组织内p42和p44 MAPK磷酸化均明显增强并有p42和p44 MAPK总蛋白表达量的增加.结论：p42/44 MAPK通路参与烟碱诱导大鼠海马CA1区LTP形成的信号转导过程.%AIM: To investigate the relationship between activation of p42/44 mitogen-activated protein kinase .(MAPK)pathway and hippocampal long term potentiation (LTP)induced by nicotine in area CA1. METHODS: Extracellular recording of population spike (PS) was performed within the pyramidal cell layer of hippocampal area CAl in vitro; Western blot analysis was employed to detect the active phosphorylated state and the total protein expression of p42/44 MAPK. RESULTS: PD98059concentration-dependently (25 μmol/L, 50 μmol/L) attenuated the induction of LTP induced by nicotine 10 μmol/L; both p42 and p44 MAPK were activated with their total protein expression increasing in CA1 subregion in response to LTP induced by nicotine. CONCLUSION: Activation of p42/44 MAPK pathway is required for hippocampal LTP induced by nicotine.
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