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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 25μmol/L和50μmol/L呈剂量依赖性抑制烟碱(10μmol/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 role of p42 / 44 MAPK pathway in nicotine-induced hippocampal CA1 region long-term potentiation (LTP) formation. Methods: The peak potentials of pyramidal cells in hippocampal CA1 region of rat hippocampal slices were recorded by extracellular field potentials. The phosphorylation of p42 / 44 MAPK and its total protein expression were detected by Western blotting. Results: PD98059 inhibited the formation of LTP in CA1 of hippocampus in a dose-dependent manner in 25μmol / L and 50μmol / L nicotine-induced nicotine (Nicotine) -induced phosphorylation of p42 and p44 MAPK in hippocampal CA1 region induced by nicotine Were significantly enhanced and p42 and p44 MAPK total protein expression increased. CONCLUSION: The p42 / 44 MAPK pathway is involved in the signal transduction of nicotine-induced LTP in the hippocampal CA1 region.