Goldberg D J, Begenisich T D, Cooper J R
J Neurobiol. 1975 Sep;6(5):453-62. doi: 10.1002/neu.480060503.
Thiamine antimetabolites were externally applied to voltage clamped squid giant axons to investigate the possible role of thiamine in nerve conduction. Phenylthiazinothiamine, in concentrations as low as 250 muM, reduced peak early current and steady-state current, with the depression of the former being two to five times greater than that of the latter. Peak transient and steady-state conductances were about equally depressed by thiamine tert-butyl disulfide (2 mM) and L-586944-00P07 (5-10 mM). None of the antimetabolites produced an appreciable change in the kinetics of Na+ activation, K+ activation, or Na+ inactivation. Thiamine itself, applied externally up to 30 mM, had no appreciable effect on either the magnitude or time course of the ionic currents. Although these data are consistent with the hypothesis that thiamine may be involved in nerve conduction, they probably reflect a nonspecific stabilizing interaction of this class of compound with the axon membrane. Taken in this light, the hypothesis that thiamine plays a direct role in Na+ channel permeability changes must be reevaluated.
将硫胺抗代谢物外用在电压钳制的枪乌贼巨轴突上，以研究硫胺在神经传导中的可能作用。浓度低至250 μM的苯基噻嗪硫胺可降低早期峰值电流和稳态电流，前者的降低幅度比后者大两到五倍。硫胺叔丁基二硫化物（2 mM）和L-586944-00P07（5 - 10 mM）对瞬态峰值电导和稳态电导的抑制作用大致相同。这些抗代谢物均未对Na⁺激活、K⁺激活或Na⁺失活的动力学产生明显影响。外用高达30 mM的硫胺本身对离子电流的大小或时程均无明显影响。尽管这些数据与硫胺可能参与神经传导的假说一致，但它们可能反映了这类化合物与轴突膜的非特异性稳定相互作用。据此，硫胺在Na⁺通道通透性变化中起直接作用的假说必须重新评估。
