Abstract: Most insecticides are potent neurotoxicants that act on various targets in the nerve systems. Organophosphorus (OP) insecticides inhibit not only acetylcholinesterase activity and acetylcholine (Ach) receptor function, affecting the release of Ach from presynaptic membrane, but also the development of nerve cells, indicating the noncholinergic effects of these insecticides. Some of the OP insecticides can induce delayed neurotoxicity in mammals. Neonicotinoid insecticides, agonists of nicotinic acetylcholine receptors (nAChRs), act on the alpha subunit of the receptors, which increases their postsynaptic potential. These kind of insecticides show selective toxicity for insects over vertebrates because they act on different subunits of the nAChRs from those in vertebrates. Pyrethroid insecticides act mainly on the sodium channels, keeping the channels open leading to the blocking of signal transmission. In addition, pyrethroids can inhibit the activity of calcium channels and interfere with the release of glutamates and dopamines. The selective toxicity of pyrethroids for insects probably resulted from configuration differences of the sodium ion channels in nerve cells between insects and mammals. Avermectin insecticides can cause the release of gammaaminobutyric acid (GABA) and enhance the affinity of GABA with GABA receptors, leading to chloride influx and postsynaptic hyperpolarization. Owing to the difficulty of penetrating the blood brain barrier to bind to GABA receptors in central nervous system (CNS) of vertebrates, the toxicity of the avermectins to vertebrates is much lower than to insects. Spinosad insecticides act not only on the nAChRs in the CNS of insects, inducing long-term release of the Ach, but also on the GABA receptors, affecting the function of GABA gated chloride ion channels.

Key words: Insecticide, neurotoxicity, ion channel, receptor, transmitter