Abstract
This chapter covers the neurophysiological mechanisms of action of various insecticides. Most insecticides are neuropoisons, but their target sites are rather limited. For example, voltage-gated sodium channels are the major target of pyrethroids and dichlorodiphenyltrichloroethane (DDT); gamma-aminobutyric acidA (GABAA) receptors are attacked by cyclodienes, hexachlorocyclohexane (HCH), and fipronil; neuronal nicotinic acetylcholine (nnACh) receptors are the target of nicotine, and nitromethylene and nitroimine heterocycles (for example, imidacloprid). Organophosphate and carbamate insecticides inhibit acetylcholinesterase. Despite apparent differences in chemical structure, pyrethroids and DDT exert similar actions on the nervous system through modulation of the function of voltage-gated sodium channels. Imidacloprid exhibits a unique mechanism of action on nicotinic acetylcholine (nACh) receptors. It binds to insect nACh receptors with a high affinity. Imidacloprid depolarized nerve membrane and caused spontaneous discharges in cockroaches. Fipronil has been found to block insect GABA receptors.
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