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为探讨中枢神经系统铅中毒的生化机制，以慢性染铅鼠为动物模型，用高频刺激诱发海马区产生长时程增强后，以Ｆｕｒａ－２为Ｃａ２＋指示剂，测定海马神经元Ｃａ２＋浓度。以放射性［ｒ－３２Ｐ］－ＡＴＰ掺入外源性底物方法测定神经元胞浆及胞膜ＰＫＣ活性。结果：染铅组长时程增强过程中Ｃａ２＋浓度明显升高（２３６．４８±６１．８３ｎｍｏｌ／Ｌ），与对照组比较有统计学意义（Ｐ＜０．００１）。ＰＫＣ活性亦升高（胞浆：１．８７±０．３５ｎｍｏｌ／ｍｇ．ｍｉｎ－１；胞膜１．５２±０．４０ｎｍｏｌ／ｍｇ．ｍｉｎ－１），与对照组比较有统计学意义（Ｐ＜０．０１；Ｐ＜０．００１）。说明海马长时程增强过程中，铅作为钙的类似物可使Ｃａ２＋浓度升高激活ＰＫＣ，进而干扰长时程增强过程。证明Ｃａ２＋－ＰＫＣ系统对铅有高度敏感性，可能是铅致神经毒性作用的关键中介物。
To explore the biochemical mechanisms of lead poisoning in the central nervous system, chronic lead poisoning rats were used as animal models. High-frequency stimulation was used to induce long-term potentiation in hippocampus. Fura-2 was used as Ca2 + indicator to determine the concentration of Ca2 + in hippocampal neurons. The radioactive [r-32P] -ATP incorporation into exogenous substrate method was used to measure the cytoplasmic and membrane PKC activity of neurons. Results: Ca2 + concentration in the lead-exposed group increased significantly (236.48 ± 61.83nmol / L) compared with the control group (P <0.001). PKC activity was also increased (cytoplasm: 1.87 ± 0.35nmol / mg.min-1; cell membrane was 1.52 ± 0.40nmol / mg.min-1), which was statistically significant compared with the control group <0.01; P <0.001). Description of hippocampal long-term potentiation process, lead as an analog of calcium Ca2 + concentration can activate PKC, thereby interfering with long-term potentiation process. Proved that Ca2 + -PKC system is highly sensitive to lead and may be the key mediator of lead-induced neurotoxicity.