Kobrinsky E M, Pearson H A, Dolphin A C
Department of Pharmacology, Royal Free Hospital School of Medicine, London, U.K.
Neuroscience. 1994 Feb;58(3):539-52. doi: 10.1016/0306-4522(94)90079-5.
The dorsal root ganglion-neuroblastoma cell line ND7-23 expresses low-voltage-activated calcium channel currents, and also expresses high-voltage-activated currents in about 50% of differentiated cells. Calcium channel currents were recorded with Ba2+ as the charge carrier. Low-voltage-activated currents were maximally activated at -30 mV and completely inactivated at holding potentials of -60 to -50 mV. omega-Conotoxin GVIA produced a reversible inhibition of low-voltage-activated currents, whereas the inhibition of high-voltage-activated current was largely irreversible. Dihydropyridine antagonists did not inhibit low-voltage-activated currents, whereas they inhibited a sustained, high-voltage-activated current. Low-voltage-activated currents were inhibited to a greater extent than high-voltage-activated currents by Ni2+ (100 microM) and by phenytoin (10 microM). Bradykinin (0.1 microM), baclofen (2 microM) and internal guanosine-5'-O-3-thiotriphosphate (100 microM) inhibited low-voltage-activated currents without affecting their kinetics of activation. Two classes of low-voltage-activated current were distinguished by their kinetics of inactivation. In the majority of cells, currents were slowly inactivating with a time-constant of inactivation of about 50 ms. They also exhibited a sustained component to the current, representing about 20% of the peak current. This component could be distinguished pharmacologically from high-voltage-activated current. The remainder of cells expressed a rapidly and completely inactivating current, with a time-constant of inactivation of about 20 ms. Two distinct single channel currents were observed in these cells, from cell-attached patch measurements, one had a single channel conductance of 7.9 pS, and the ensemble average current showed some inactivation. It is likely that this channel subtype underlies the low-voltage-activated current. The other showed long openings in the presence of a dihydropyridine agonist, had a conductance of 23.1 pS, and was non-inactivating.
背根神经节-神经母细胞瘤细胞系ND7-23表达低电压激活的钙通道电流，并且在约50%的分化细胞中也表达高电压激活电流。以Ba2+作为电荷载体记录钙通道电流。低电压激活电流在-30 mV时达到最大激活，并在-60至-50 mV的钳制电位下完全失活。ω-芋螺毒素GVIA对低电压激活电流产生可逆性抑制，而对高电压激活电流的抑制在很大程度上是不可逆的。二氢吡啶拮抗剂不抑制低电压激活电流，而抑制持续性的高电压激活电流。Ni2+（100 microM）和苯妥英（10 microM）对低电压激活电流的抑制程度大于对高电压激活电流的抑制。缓激肽（0.1 microM）、巴氯芬（2 microM）和胞内鸟苷-5'-O-3-硫代三磷酸（100 microM）抑制低电压激活电流而不影响其激活动力学。根据失活动力学区分出两类低电压激活电流。在大多数细胞中，电流缓慢失活，失活时间常数约为50 ms。它们还表现出电流的持续性成分，约占峰值电流的20%。该成分在药理学上可与高电压激活电流区分开。其余细胞表达快速且完全失活的电流，失活时间常数约为20 ms。通过细胞贴附膜片钳测量在这些细胞中观察到两种不同的单通道电流，一种单通道电导为7.9 pS，整体平均电流表现出一些失活。这种通道亚型可能是低电压激活电流的基础。另一种在存在二氢吡啶激动剂时表现出长开放，电导为23.1 pS，且无失活。
