Madeja M, Musshoff U, Binding N, Witting U, Speckmann E J
Institut für Physiologie, D-48149 Muenster, Germany.
J Neurophysiol. 1997 Nov;78(5):2649-54. doi: 10.1152/jn.1997.78.5.2649.
Effects of Pb2+ on delayed-rectifier potassium channels in acutely isolated hippocampal neurons. J. Neurophysiol. 78: 2649-2654, 1997. The effects of Pb2+ on delayed-rectifier potassium currents were studied in acutely isolated hippocampal neurons (CA1 neurons, CA3 neurons, granule cells) from the guinea pig using the patch-clamp technique in the whole cell configuration. Pb2+ in micromolar concentrations decreased the potassium currents in a voltage-dependent manner, which appeared as a shift of the current-voltage relation to positive potentials. The effect was reversible after washing. The concentration-responsiveness measured in CA1 neurons revealed an IC50 value of 30 mu mol/l at a potential of -30 mV. The half-maximal shift of the current-voltage relation was reached at 33 mu mol/l and the maximal obtainable shift was 13.4 mV. For the different types of hippocampal neurons, the shift of the current-voltage relation was distinct and was 7.9 mV in CA1 neurons, 13.7 mV in CA3 neurons, and 14.2 mV in granule cells with 50 micro mol/l Pb2+. The effects described here of Pb2+ on the potassium currents in hippocampal neurons and the differences between the types of hippocampal neurons correspond with the known properties and distributions of cloned potassium channels found in the hippocampus. As a whole, our results demonstrate that Pb2+ in micromolar concentration is a voltage-dependent, reversible blocker of delayed-rectifier potassium currents of hippocampal neurons. This effect has to be taken into consideration as a possible contributing mechanism for the neurological symptoms of enhanced brain activity seen during Pb2+ intoxication.
铅离子对急性分离的海马神经元中延迟整流钾通道的影响。《神经生理学杂志》78: 2649 - 2654, 1997年。采用全细胞模式的膜片钳技术，研究了铅离子对豚鼠急性分离海马神经元（CA1神经元、CA3神经元、颗粒细胞）中延迟整流钾电流的影响。微摩尔浓度的铅离子以电压依赖的方式降低钾电流，表现为电流 - 电压关系向正电位偏移。洗脱后该效应可逆。在CA1神经元中测量的浓度 - 反应性显示，在 - 30 mV电位下IC50值为30 μmol/l。电流 - 电压关系的半最大偏移在33 μmol/l时达到，最大可获得偏移为13.4 mV。对于不同类型的海马神经元，电流 - 电压关系的偏移各不相同，在50 μmol/l铅离子作用下，CA1神经元中为7.9 mV，CA3神经元中为13.7 mV，颗粒细胞中为14.2 mV。本文所述的铅离子对海马神经元钾电流的影响以及海马神经元类型之间的差异，与海马中克隆的钾通道的已知特性和分布相符。总体而言，我们的结果表明，微摩尔浓度的铅离子是海马神经元延迟整流钾电流的电压依赖性、可逆性阻滞剂。这种效应必须被视为铅离子中毒期间所见脑活动增强的神经症状的一种可能促成机制。
