Fejtl M, Györi J, Carpenter D O
Wadsworth Center for Laboratories and Research, New York State Dept. of Health, Albany 12201-0509.
Neuroreport. 1994 Nov 21;5(17):2317-20. doi: 10.1097/00001756-199411000-00027.
Carbachol and acetylcholine (ACh)-activated whole-cell chloride currents were recorded in identified neurons of Aplysia californica. Application of 0.1-10 microM HgCl2 potentiated the chloride response and reduced the rate of desensitization. To investigate the underlying mechanism we recorded single chloride channels in a cell-attached patch configuration. Recordings were performed successively on the same neuron with 1 microM carbachol and with 1 microM carbachol + 1 microM HgCl2, respectively. The slope conductance did not change significantly, but there was a manyfold increase in the open probability, Po. This may underlie the Hg(2+)-induced enhancement of carbachol- and ACh-evoked chloride currents in Aplysia neurons and may serve as a model for the neurotoxic effect of Hg2+ on the mammalian ACh receptor.
在加州海兔已鉴定的神经元中记录了卡巴胆碱和乙酰胆碱（ACh）激活的全细胞氯离子电流。施加0.1 - 10微摩尔的氯化汞可增强氯离子反应并降低脱敏速率。为了研究其潜在机制，我们在细胞贴附式膜片钳配置下记录了单个氯离子通道。分别在同一神经元上先后用1微摩尔卡巴胆碱和1微摩尔卡巴胆碱 + 1微摩尔氯化汞进行记录。斜率电导没有显著变化，但开放概率Po增加了许多倍。这可能是汞（2 +）诱导的海兔神经元中卡巴胆碱和ACh诱发的氯离子电流增强的基础，并且可能作为汞2 +对哺乳动物ACh受体神经毒性作用的模型。
