Abstract
This chapter describes several electrophysiological targets of pesticides, including the voltage-gated sodium channel, acetylcholine receptors, and the GABAA receptors, covering the neurophysiological mechanisms of action of various insecticides. The understanding of these interactions between several classes of pesticides, including the pyrethroids and organophosphate and carbamate insecticides, and these biological systems allows for the determination of the most sensitive biological component (e.g., ionic channel) but also the development of preventive strategies. Applications of molecular biology and genetics techniques have made it possible to identify the molecular species that are responsible for the toxic action of insecticides, particularly those related to the target resistance of insects to insecticides. Most insecticides are neuropoisons, but their target sites are rather limited. Voltage-gated sodium channels are the major target of pyrethroids and DDT; GABAA receptors are attacked by cyclodienes, hexachlorocyclohexane (HCH), and fipronil; neuronal nicotinic acetylcholine (nnACh) receptors are the target of nicotine, and nitromethylene and nitroimine hete-rocycles (e.g., imidacloprid). Organophosphate and carbamate insecticides inhibit acetylcholinesterase.
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