Legros C, Martin-Eauclaire MF, Cattaert D
Laboratoire de Biochimie, Unite Mixte de Recherche 6560 du Centre National de la Recherche Scientifique, Institut Federatif de Recherche Jean Roche, Universite de la Mediterranee, Faculte de Medecine Secteur Nord, Boulevard Pierre Drama.
J Exp Biol. 1998 Sep;201 (Pt 18):2625-36. doi: 10.1242/jeb.201.18.2625.
The resistance of the scorpion Androctonus australis to its own venom, as well as to the venom of other species, was investigated. A comparison of the electrical and pharmacological properties of muscle and nerve fibres from Androctonus australis with those from the crayfish Procambarus clarkii enabled us to understand the lack of effect of scorpion venom (110-180 microg ml-1) and purified toxins, which are active on voltage-gated Na+ and K+ channels, Ca2+-activated K+ channels, on scorpion tissues. Voltage-clamp experiments showed that peptide K+ channel blockers from scorpion and snake have no effect on currents in muscle and nerve fibres from either scorpions or crayfish. The scorpion toxin kaliotoxin (KTX), a specific blocker of Kv1.1 and Kv1.3 K+ channels, had no effect on muscle fibres of A. australis (2 micromol l-1) or P. clarkii (400 nmol l-1). Similarly, charybdotoxin (ChTX) had no effect on the muscle fibres of A. australis (10 micromol l-1) or P. clarkii (200 nmol l-1) and neither did the snake toxin dendrotoxin (DTX) at concentrations of 100 nmol l-1 in A. australis and 200 nmol l-1 in P. clarkii. These three toxins (KTX, ChTX and DTX) did not block K+ currents recorded from nerve fibres in P. clarkii. The pharmacology of the K+ channels in these two arthropods did not conform to that previously described for K+ channels in other species. Current-clamp experiments clearly indicated that the venom of A. australis (50 microg ml-1) had no effect on the shape of the action potential recorded from nerve cord axons from A. australis. At a concentration of 50 microg ml-1, A. australis venom greatly prolonged the action potential in the crayfish giant axon. The absence of any effect of the anti-mammal 
-toxin AaH II (100 nmol l-1) and the anti-insect toxin AaH IT1 (100 nmol l-1) on scorpion nerve fibres revealed strong pharmacological differences between the voltage-gated Na+ channels of scorpion and crayfish. We conclude that the venom from A. australis is pharmacologically inactive on K+ channels and on voltage-sensitive Na+ channels from this scorpion.
对澳大利亚杀人蝎对自身毒液以及其他物种毒液的抗性进行了研究。将澳大利亚杀人蝎与克氏原螯虾的肌肉和神经纤维的电学和药理学特性进行比较，使我们能够理解蝎毒（110 - 180微克/毫升）和纯化毒素对蝎组织缺乏作用的原因，这些毒素对电压门控的Na⁺和K⁺通道、Ca²⁺激活的K⁺通道具有活性。电压钳实验表明，来自蝎子和蛇的肽类K⁺通道阻滞剂对蝎子或小龙虾的肌肉和神经纤维中的电流没有影响。蝎毒素卡利毒素（KTX）是Kv1.1和Kv1.3 K⁺通道的特异性阻滞剂，对澳大利亚杀人蝎（2微摩尔/升）或克氏原螯虾（400纳摩尔/升）的肌肉纤维没有影响。同样，查利毒素（ChTX）对澳大利亚杀人蝎（10微摩尔/升）或克氏原螯虾（200纳摩尔/升）的肌肉纤维没有影响，蛇毒素树突毒素（DTX）在澳大利亚杀人蝎中浓度为100纳摩尔/升、在克氏原螯虾中浓度为200纳摩尔/升时也没有影响。这三种毒素（KTX、ChTX和DTX）并未阻断克氏原螯虾神经纤维中记录到的K⁺电流。这两种节肢动物中K⁺通道的药理学特性与先前描述的其他物种中的K⁺通道不同。电流钳实验清楚地表明，澳大利亚杀人蝎的毒液（50微克/毫升）对从澳大利亚杀人蝎神经索轴突记录到的动作电位的形状没有影响。在浓度为50微克/毫升时，澳大利亚杀人蝎毒液极大地延长了小龙虾巨轴突中的动作电位。抗哺乳动物α-毒素AaH II（100纳摩尔/升）和抗昆虫毒素AaH IT1（100纳摩尔/升）对蝎神经纤维没有任何影响，这揭示了蝎子和小龙虾的电压门控Na⁺通道之间存在很强的药理学差异。我们得出结论，澳大利亚杀人蝎的毒液在药理学上对该蝎子的K⁺通道和电压敏感Na⁺通道无活性。
