Lee D, Park Y, Brown T M, Adams M E
Department of Entomology and Neuroscience, University of California, Riverside 92521, USA.
Mol Pharmacol. 1999 Mar;55(3):584-93.
Genetic resistance to pyrethroid insecticides involves nervous system insensitivity linked to regulatory and structural genes of voltage-sensitive sodium channels. We examined the properties and relative density of sodium channels in central neurons of susceptible and pyrethroid-resistant (Pyr-R) insects that were homozygous for the amino acid substitution V421M in the I-S6 transmembrane segment. Pyr-R sodium channels show approximately 21-fold lower sensitivity to the synthetic pyrethroid permethrin and a approximately 2-fold increased sensitivity to the alpha-scorpion toxin LqhalphaIT. Pyr-R channels also exhibit altered gating properties, including a approximately 13 mV positive shift in voltage-dependent activation and approximately 7 mV positive shift in steady-state inactivation. Consistent with these changes in gating behavior, Pyr-R central neurons are less excitable, as evidenced by an approximately 11 mV elevation of action potential threshold. No differences in sodium channel density are evident. The altered properties of Pyr-R sodium channels provide a plausible molecular basis for nervous system insensitivity associated with pyrethroid resistance.
对拟除虫菊酯类杀虫剂的遗传抗性涉及与电压敏感性钠通道的调控基因和结构基因相关的神经系统不敏感性。我们研究了在I-S6跨膜区段存在氨基酸替代V421M的纯合易感昆虫和拟除虫菊酯抗性(Pyr-R)昆虫的中枢神经元中钠通道的特性和相对密度。Pyr-R钠通道对合成拟除虫菊酯氯菊酯的敏感性降低约21倍,对α-蝎毒素LqhalphaIT的敏感性增加约2倍。Pyr-R通道还表现出改变的门控特性,包括电压依赖性激活正向偏移约13 mV,稳态失活正向偏移约7 mV。与这些门控行为的变化一致,Pyr-R中枢神经元的兴奋性较低,动作电位阈值升高约11 mV证明了这一点。钠通道密度没有明显差异。Pyr-R钠通道特性的改变为与拟除虫菊酯抗性相关的神经系统不敏感性提供了一个合理的分子基础。