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目的:观察钙离子在烟碱诱导的大鼠海马脑片CA_1区长时程增强中的作用。方法:细胞外记录离体海马脑片CA_1区锥体细胞层群体峰电位。结果:至少烟碱1μmol·L~(-1)可诱导海马CA_1区长时程增强形成。移去脑脊液中的钙离子,烟碱不能诱导CA_1区长时程增强形成。硝苯地平1与10μmol·L~(-1)部分抑制而Tharpsigargin 1与10μmol·L~(-1)完全抑制烟碱诱导的长时程增强形成。结论:烟碱诱导的海马CA_1区长时程增强呈钙离子依赖性,胞外钙内流和胞内钙释放都参与了长时程增强形成。
Objective: To observe the effect of calcium ion on nicotine-induced long-term potentiation of CA 1 region in rat hippocampal slices. Methods: The peak potentials of CA1 pyramidal cells in isolated rat hippocampal slices were recorded extracellularly. Results: At least nicotine 1μmol·L -1 could induce long-term potentiation of hippocampal CA 1 region formation. Removal of calcium in cerebrospinal fluid, nicotine can not induce long-term potentiation of CA 1 area formation. Nifedipine 1 and 10 μmol·L -1 partial inhibition while Tharpsigargin 1 and 10 μmol·L -1 completely inhibited nicotine-induced long-term potentiation. CONCLUSION: Nicotine-induced long-term potentiation of hippocampal CA 1 region is calcium-dependent, extracellular calcium influx and intracellular calcium release are involved in long-term potentiation.