Audesirk G, Audesirk T
Biology Department, University of Colorado, Denver 80204.
Neurotoxicology. 1989 Winter;10(4):659-69.
The effects of acute in vitro lead exposure on slowly inactivating voltage-sensitive calcium channels in central neurons of the freshwater pond snail Lymnaea stagnalis were studied under voltage clamp. Three physiologically distinct cell types were used: two subsets of the B cell cluster (Bpos and Bneg) and the pedal giant neuron (RPeD1). In Bpos neurons, 5 nM free Pb2+ irreversibly inhibited current flow through calcium channels by 38 +/- 10%. In Bneg neurons, 5 nM free Pb2+ slightly inhibited inward currents (12 +/- 6%) and may have shifted their voltage dependence to more depolarized voltages. The inhibition and voltage shift were irreversible. In RPeD1 neurons, Pb2+ caused a small, statistically insignificant inhibition of inward current (5 nM free Pb2+; 18 +/- 19%; 30 nM free Pb2+: 31 +/- 23%). The effects of Pb2+ were fully reversible. These data indicate that (1) voltage-sensitive calcium channels in Lymnaea neurons are inhibited by nanomolar concentrations of free Pb2+; (2) there are multiple types of calcium channels in Lymnaea neurons; and (3) the effects of in vitro lead exposure differ qualitatively among channel types.
在电压钳制条件下,研究了急性体外铅暴露对淡水池塘蜗牛椎实螺中枢神经元中缓慢失活的电压敏感性钙通道的影响。使用了三种生理上不同的细胞类型:B细胞簇的两个亚群(Bpos和Bneg)以及足神经节巨型神经元(RPeD1)。在Bpos神经元中,5 nM游离Pb2+不可逆地抑制通过钙通道的电流,抑制率为38±10%。在Bneg神经元中,5 nM游离Pb2+轻微抑制内向电流(12±6%),并可能使其电压依赖性向更去极化的电压偏移。这种抑制和电压偏移是不可逆的。在RPeD1神经元中,Pb2+对内向电流产生了微小的、统计学上不显著的抑制(5 nM游离Pb2+;18±19%;30 nM游离Pb2+:31±23%)。Pb2+的作用是完全可逆的。这些数据表明:(1)椎实螺神经元中的电压敏感性钙通道受到纳摩尔浓度游离Pb2+的抑制;(2)椎实螺神经元中有多种类型的钙通道;(3)体外铅暴露对不同通道类型的影响在性质上有所不同。