镉对骨骼神经肌肉传递的药理作用。

The pharmacological effects of cadmium on skeletal neuromuscular transmission.

Braga M F, Rowan E G

Department of Physiology and Pharmacology, Strathclyde Institute for Drug Research, University of Strathclyde, Glasgow, Scotland.

Gen Pharmacol. 1994 Dec;25(8):1729-39. doi: 10.1016/0306-3623(94)90379-4.

Abstract

Cadmium (100 microM) blocks neuromuscular transmission by blocking prejunctional voltage dependent calcium channels in a competitive manner. 2. Prolonged exposure to cadmium leads to a block of neuromuscular transmission that is not competitive. 3. Cadmium can increase the spontaneous release of acetylcholine, this release is modified by the cation composition of the bathing solution. 4. Cadmium may enter the nerve terminal via the voltage dependent calcium channels (the L-type calcium channel has been implicated) and exert some of its actions intracellularly. 5. All of the extracellular effects of cadmium can be reversed by cysteine.

摘要

镉（100微摩尔）通过竞争性阻断接头前电压依赖性钙通道来阻断神经肌肉传递。2. 长期暴露于镉会导致非竞争性的神经肌肉传递阻滞。3. 镉可增加乙酰胆碱的自发释放，这种释放会因灌流液的阳离子成分而改变。4. 镉可能通过电压依赖性钙通道（涉及L型钙通道）进入神经末梢，并在细胞内发挥一些作用。5. 镉的所有细胞外效应都可被半胱氨酸逆转。