Purkerson S L, Baden D G, Fieber L A
University of Miami Rosenstiel School of Marine and Atmospheric Science, Division of Marine Biology and Fisheries, NIEHS Marine and Freshwater Biomedical Sciences Center, FL 33149, USA.
Neurotoxicology. 1999 Dec;20(6):909-20.
Single Na+ channel currents were recorded from cell-attached membrane patches from two neuronal cell lines derived from rat brain, B50 and B104, and compared before and after exposure of the cells to purified brevetoxin, PbTx-3. B50 and B104 Na+ channels usually exhibited fast activation and inactivation as is typical of TTX-sensitive Na+ channels. PbTx-3 modified channel gating in both cell lines. PbTx-3 caused (1) significant increases in the frequency of channel reopening, indicating a slowing of channel inactivation, (2) a change in the voltage dependence of the channels, promoting channel opening during steady-state voltage clamp of the membrane at voltages throughout the activation range of Na+ currents, but notably near the resting potential of these cells (-60 - -50 mV), and (3) a significant, 6.7 mV hyperpolarized shift in the threshold potential for channel opening. Na+ channel slope conductance did not change in PbTx-3-exposed B50 and B104 neurons. These effects of Pbx-3 may cause hyperexcitability as well as inhibitory effects in intact brain.
从源自大鼠脑的两种神经元细胞系B50和B104的细胞贴附膜片上记录单个钠离子通道电流，并在细胞暴露于纯化的短裸甲藻毒素PbTx-3之前和之后进行比较。B50和B104钠离子通道通常表现出快速激活和失活，这是TTX敏感钠离子通道的典型特征。PbTx-3改变了两种细胞系中的通道门控。PbTx-3导致：（1）通道重新开放频率显著增加，表明通道失活减慢；（2）通道电压依赖性改变，在整个钠离子电流激活范围内的膜稳态电压钳制期间促进通道开放，但在这些细胞的静息电位（-60 - -50 mV）附近尤为明显；（3）通道开放阈值电位发生6.7 mV的显著超极化偏移。在暴露于PbTx-3的B50和B104神经元中，钠离子通道斜率电导没有变化。PbTx-3的这些作用可能在完整大脑中引起兴奋性过高以及抑制作用。
