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蔡原, 刘秋芳, 张颖花, 郭纳新, 奚奇, 万伯健. 慢性染铅对大鼠脑海马齿状回长时程增强的抑制作用及其机理探讨[J]. 中国公共卫生, 2000, 16(3): 230-232. DOI: 10.11847/zgggws2000-16-03-30
引用本文: 蔡原, 刘秋芳, 张颖花, 郭纳新, 奚奇, 万伯健. 慢性染铅对大鼠脑海马齿状回长时程增强的抑制作用及其机理探讨[J]. 中国公共卫生, 2000, 16(3): 230-232. DOI: 10.11847/zgggws2000-16-03-30
Cai Yuan, . Inhibition Effect of Chronic Lead Exposure on LTP in Rat Hippocampal Dentate Gyrus and Its Mechanism Exploration[J]. Chinese Journal of Public Health, 2000, 16(3): 230-232. DOI: 10.11847/zgggws2000-16-03-30
Citation: Cai Yuan, . Inhibition Effect of Chronic Lead Exposure on LTP in Rat Hippocampal Dentate Gyrus and Its Mechanism Exploration[J]. Chinese Journal of Public Health, 2000, 16(3): 230-232. DOI: 10.11847/zgggws2000-16-03-30

慢性染铅对大鼠脑海马齿状回长时程增强的抑制作用及其机理探讨

Inhibition Effect of Chronic Lead Exposure on LTP in Rat Hippocampal Dentate Gyrus and Its Mechanism Exploration

  • 摘要: 给刚断乳的大鼠饮用02%醋酸铅水90~108d后,测定血铅和脑铅水平、脑海马齿状回LTP的诱发率、神经元内Ca2+浓度和细胞膜和胞液中蛋白激酶C活性,以探讨铅损害学习记忆功能的机理.结果:实验组动物血铅(4.76±1.08μmol/L)和脑铅(0.59±0.06μg/g湿重)水平明显高于对照组(分别为0.17±0.08μmol/L和0.06±0.02μg/g湿重)(P<0.01);诱发的LTP发生率为18.2%(2/11),明显低于对照组的83.3%(10/12)(P<0.01),发生LTP动物的PS幅值增长率为基线值(按10.0%计)的120.15±7.15%,明显低于对照组的142.70±15.10%(P<0.05),另有63.6%(7/11)的动物出现长时程抑制(LTD);染铅大鼠海马神经元的Ca2+浓度、胞膜和胞液PKC活性分别为265.48±53.61mmol/L、1.52±0.40和1.87±0.35nmol/min/mg蛋白,均比对照组(为108.81±26.85mmol/L、0.94±0.33和131±0.29nmol/min/mg蛋白)显着升高(P<0.01).这表明,慢性染铅损害LTP的形成,而海马神经元Ca2+浓度和PKC活性的异常增高可能是重要机理之一.

     

    Abstract: After the weanling male Wistar rats were fed 0.2% acetate lead water for 90~108 days,blood lead and brain blood lead,the induction rate of LTP,the concentration of Ca2+ and the activities of protein kinase C(PKC) in the neurons of rathippocampal dentate gyrus(DG) were measured in order to probe into the mechanisms of lead induced impairment on learning and memory functions.The results showed that blood lead(4.76±1.08μmol/L) and brain blood lead(0.59±0.06μg/g tissue)in rats of the tested group were obviously higher than that in the control(0.17±0.08μmol/L and 0.06±0.02μg/g tissue,respectively)(P<0.01);the induction rate of LTP and the changes of PS amplitude in the tested group were only 18.2%(2/11) and 120.15±7.15% respectively,and statistically lower than 83.3%(10/12)and 142.70±15.10% in the control(P<0.01 and P<0.05,respectively).Besides that,7 rats in the tested group occured LTD(63.6%).The Ca2+ concentration and the PKC activities in cytosol and membrane of hippocampal neurons from lead exposed rats(265.48±53.61mmol/L、1.52±0.40 and 1.87±0.35nmol/min/mg protein,respectively)all significantly increased when comparing with the control(108.81±26.85mmol/L、0.94±0.33 and 1.31±0.29nmol/min/mg protein,respectively)(P<0.01).These results demonstrated that chronic lead exposure can cause adverse effects to the formation of LTP,and suggested that the aberrant increases of Ca2+ concentration and the PKC activities in hippocampal neurons may play an importent role in LTP process disturbance associated with lead.

     

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