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给刚断乳的大鼠饮用 0 2 %醋酸铅水 90～ 10 8d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 0 8μmol/L)和脑铅 (0 5 9± 0 0 6 μg/ g湿重 )水平明显高于对照组 (分别为 0 17± 0 0 8μmol/L和 0 0 6± 0 0 2 μg/g湿重 ) (P<0 0 1) ;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 0 1) ,发生LTP动物的PS幅值增长率为基线值 (按 10 0 %计 )的 12 0 15± 7 15 % ,明显低于对照组的 142 70± 15 10 % (P <0 0 5 ) ,另有 6 3 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 2 6 5 48± 5 3 6 1mmol/L、1 5 2±0 40和 1 87± 0 35nmol/min/mg蛋白 ,均比对照组 (为 10 8 81± 2 6 85mmol/L、0 94± 0 33和 1 31± 0 2 9nmol/min/mg蛋白 )显著升高 (P <0 0 1)。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。
The rats were weaned with 0 2% lead acetate 90 to 108 days after weaning, and the levels of blood lead and brain lead, the induction rate of LTP in the hippocampus, the Ca2 + concentration in the neurons and the protein in the cell membrane and cytosol Kinase C activity to explore the mechanism of lead damage to learning and memory. Results: The levels of blood lead (4 76 ± 1 0 8 μmol / L) and brain lead (0 59 ± 0 0 6 μg / g wet weight) in the experimental group were significantly higher than those in the control group (0 17 ± 0 0 8μmol / L and 0 0 6 ± 0 2 μg / g wet weight) (P <0.01). The incidence of induced LTP was 18 2% (2/11) and significantly lower than that of the control group 83 3% (10 / 12) (P <0.01). The rate of increase in PS amplitude of LTP animals was 12 0 15 ± 7 15% of the baseline value (100%), which was significantly lower than that of the control group 142 70 ± 15 10% (P <0 05), and 6 36% (7/11) of animals showed long-term inhibition (LTD). Ca2 + concentrations in the hippocampus neurons of lead-exposed rats, respectively, Were 565 ± 5 361 mmol / L, 1 52 ± 0 40 and 1 87 ± 0 35 nmol / min / mg protein, which were significantly higher than that of the control group (10 8 81 ± 2 6 85 mmol / L, 0 94 ± 0 33 and 1 31 ± 0 29 nmol / min / mg protein) were significantly increased (P <0.01). This suggests that chronic lead poisoning impairs the formation of LTP, and that abnormal increase in Ca2 + concentration and PKC activity in hippocampal neurons may be one of the important mechanisms.