Abstract: The voltage-gated sodium channels of insects exist on the membrane of all excitable cells. Because of their essential role in the generation and transmission of potential action and electrical signaling in excitable cells, sodium channels are the target site of the organochlorine and pyrethroid insecticides. Due to massive use of organochlorines and pyrethroids for the control of agricultural and medical insect pests, the number of insect pests that have developed resistance to these insecticides is drastically increasing. One major mechanism of the resistance is known as knock-down resistance (kdr). Insects exhibiting kdr have reduced target-site (sodium channel) sensitivity to organochlorines and pyrethroids, mainly resulting from one or more nonsynonymous point mutations in the insect sodium channel protein. In this article, we reviewed the transmembrane topology structure, function, evolution and gene cloning of voltage-gated sodium channels. More importantly, we summarized the known 40 nonsynonymous mutations from more than 40 insect species, the mRNA alternative splicing and editing of the sodium channel genes, and their association with insecticide resistance. We also reviewed the insecticide resistance mechanisms due to protein structure changes resulting from these mutations. These researches provide a comprehensive information frame for further identification of mutations and molecular mechanisms associated with organochlorine and pyrethroid resistance, and the development of molecular monitoring methods of the resistance.

Key words: Sodium channel, kdr mutation, RNA splicing and editing, insecticide resistance, protein structure, resistance monitoring