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铅会抑制海兔神经元的电压激活钙电流。

Lead inhibits the voltage-activated calcium current of Aplysia neurons.

作者信息

Büsselberg D, Evans M L, Rahmann H, Carpenter D O

机构信息

Wadsworth Center for Laboratories and Research, New York State Department of Health and School of Public Health, Albany 12201.

出版信息

Toxicol Lett. 1990 Mar;51(1):51-7. doi: 10.1016/0378-4274(90)90224-a.

Abstract

Lead is a potent and reversible inhibitor of the voltage-dependent calcium current of Aplysia neurons in a concentration range (1-1000 microM) similar to that which elicits toxic effects in man. The threshold for inhibition is 1 microM and the dissociation constant about 90 microM. The inhibition is due to reduction of the peak current amplitude, and not due to alteration of the voltage dependence of the activation or inactivation. The effect of lead is specific to the calcium current as the delayed rectifier potassium and the sodium currents are not affected by concentrations of lead (200 microM) which give near-maximal inhibition. The calcium current of Aplysia neurons appears similar to the current flowing through the mammalian L-type calcium channel. This suggests that inhibition of the investigated calcium channel may contribute to the toxic effects of lead in mammals.

摘要

铅是海兔神经元电压依赖性钙电流的一种强效且可逆的抑制剂,其浓度范围(1-1000微摩尔)与在人体引发毒性作用的浓度范围相似。抑制阈值为1微摩尔,解离常数约为90微摩尔。这种抑制是由于峰值电流幅度降低,而非激活或失活的电压依赖性改变所致。铅的作用对钙电流具有特异性,因为延迟整流钾电流和钠电流不受能产生近最大抑制作用的铅浓度(200微摩尔)的影响。海兔神经元的钙电流似乎与流经哺乳动物L型钙通道的电流相似。这表明所研究的钙通道受到抑制可能是铅对哺乳动物产生毒性作用的原因之一。

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