Tibbs G R, Nicholls D G, Dolly J O
Department of Biochemistry, Imperial College of Science and Technology, London, England.
FEBS Lett. 1989 Sep 11;255(1):159-62. doi: 10.1016/0014-5793(89)81081-6.
Nanomolar concentrations of charybdotoxin or dendrotoxin increase the cytoplasmic free Ca2+ concentration in isolated central nerve terminals. The effects of the two toxins, normally considered to be blockers of K+ channels controlled by voltage in a Ca2+-sensitive or -insensitive manner, respectively, show only marginal additivity. Apamin, and inhibitor of low conductance Ca2+-activated K+ channels, was without effect in either the absence or presence of dendrotoxin. The effect of charybdotoxin on polarized, isolated central nerve terminals seems to be mediated largely by a block of K+ channels sensitive to dendrotoxin. Apparently, these voltage-operated K+ channels make a more significant contribution to maintaining the polarized potential of synaptosomes than do those activated by Ca2+.
纳摩尔浓度的蝎毒素或树突毒素可增加分离出的中枢神经末梢中的细胞质游离钙离子浓度。通常认为这两种毒素分别以对钙离子敏感或不敏感的方式阻断电压门控钾通道,但其作用仅表现出微弱的相加性。蜂毒明肽是一种低电导钙离子激活钾通道的抑制剂,无论有无树突毒素存在,它都没有作用。蝎毒素对极化的、分离出的中枢神经末梢的作用似乎主要是通过阻断对树突毒素敏感的钾通道介导的。显然,这些电压门控钾通道对维持突触体的极化电位的贡献比钙离子激活的钾通道更大。