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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Domann R, Wunder L, Büsselberg D

Physiologisches Institut II, Heinrich-Heine Universität, Düsseldorf, Germany.

Cell Mol Neurobiol. 1997 Jun;17(3):305-14. doi: 10.1023/a:1026342318006.

Cultured dorsal root ganglion of rat pups were depolarized by exposure to 50 mM K+ and the rise of [Ca2+]i was measured using fura-2 as an indicator. 2. Lead in the extracellular solution reduced the rise of [Ca2+]i in a concentration-dependent manner, with a threshold concentration of 0.25 microM. More than 80% of the calcium entry was prevented by approximately 5 microM lead. The IC50 and the Hill coefficient were 3.1 microM and 1, respectively. 3. This effect was considered to be due to a reduction of VACCCs, since applications of NMDA did not result in any rise of [Ca2+]i. 4. Since Pb2+ itself changes the fura-2 signal in a typical and characteristic manner, fura-2 is also an indicator for Pb2+. No changes in fura-2 signals were detected when lead (5 microM) was applied for several minutes in the absence of calcium, indicating that Pb2+ did not enter the cells. 5. Thus it is concluded that lead prevents calcium entry by reducing VACCCs but does not cross the cell membrane itself.

将大鼠幼崽的背根神经节进行培养，通过暴露于50 mM K⁺使其去极化，并使用fura - 2作为指示剂测量细胞内钙离子浓度（[Ca²⁺]i）的升高。2. 细胞外溶液中的铅以浓度依赖性方式降低[Ca²⁺]i的升高，阈值浓度为0.25 μM。约5 μM的铅可阻止超过80%的钙内流。半数抑制浓度（IC50）和希尔系数分别为3.1 μM和1。3. 由于应用N - 甲基 - D - 天冬氨酸（NMDA）未导致[Ca²⁺]i升高，因此认为这种效应是由于电压门控性钙通道（VACCCs）减少所致。4. 由于Pb²⁺本身以典型且特征性的方式改变fura - 2信号，fura - 2也是Pb²⁺的指示剂。在无钙情况下施加铅（5 μM）几分钟后，未检测到fura - 2信号变化，表明Pb²⁺未进入细胞。5. 因此得出结论，铅通过减少VACCCs来阻止钙内流，但自身不会穿过细胞膜。

Domann R, Wunder L, Büsselberg D

Physiologisches Institut II, Heinrich-Heine Universität, Düsseldorf, Germany.

Cell Mol Neurobiol. 1997 Jun;17(3):305-14. doi: 10.1023/a:1026342318006.

Cultured dorsal root ganglion of rat pups were depolarized by exposure to 50 mM K+ and the rise of [Ca2+]i was measured using fura-2 as an indicator. 2. Lead in the extracellular solution reduced the rise of [Ca2+]i in a concentration-dependent manner, with a threshold concentration of 0.25 microM. More than 80% of the calcium entry was prevented by approximately 5 microM lead. The IC50 and the Hill coefficient were 3.1 microM and 1, respectively. 3. This effect was considered to be due to a reduction of VACCCs, since applications of NMDA did not result in any rise of [Ca2+]i. 4. Since Pb2+ itself changes the fura-2 signal in a typical and characteristic manner, fura-2 is also an indicator for Pb2+. No changes in fura-2 signals were detected when lead (5 microM) was applied for several minutes in the absence of calcium, indicating that Pb2+ did not enter the cells. 5. Thus it is concluded that lead prevents calcium entry by reducing VACCCs but does not cross the cell membrane itself.

将大鼠幼崽的背根神经节进行培养，通过暴露于50 mM K⁺使其去极化，并使用fura - 2作为指示剂测量细胞内钙离子浓度（[Ca²⁺]i）的升高。2. 细胞外溶液中的铅以浓度依赖性方式降低[Ca²⁺]i的升高，阈值浓度为0.25 μM。约5 μM的铅可阻止超过80%的钙内流。半数抑制浓度（IC50）和希尔系数分别为3.1 μM和1。3. 由于应用N - 甲基 - D - 天冬氨酸（NMDA）未导致[Ca²⁺]i升高，因此认为这种效应是由于电压门控性钙通道（VACCCs）减少所致。4. 由于Pb²⁺本身以典型且特征性的方式改变fura - 2信号，fura - 2也是Pb²⁺的指示剂。在无钙情况下施加铅（5 μM）几分钟后，未检测到fura - 2信号变化，表明Pb²⁺未进入细胞。5. 因此得出结论，铅通过减少VACCCs来阻止钙内流，但自身不会穿过细胞膜。