Abstract
Recent advances in molecular neurobiology have provided an unprecedented insight into the structure and function of the three principal target sites for neurotoxic insecticides: acetylcholinesterase, the 4-aminobutyric acid (GABA) receptor–chloride ionophore complex, and the voltage-sensitive sodium channel. This paper reviews some of these advances and their current or potential application to problems in insecticide resistance. It particularly emphasizes studies of the molecular biology of voltage-dependent sodium channels in the context of resistance to DDT and pyrethroids resulting from reduced neuronal sensitivity.
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