Most insecticides are neurotoxicants causing various forms of hyperexcitation and paralysis in animals. A variety of neuroreceptors and ion channels have been identified as the major target sites of these neurotoxic insecticides. This paper gives the highlights of some of the recent development in this area. Pyrethroids keep the sodium channel open for unusually long times causing a prolonged flow of sodium current. The prolonged sodium current elevates and prolongs the depolarizing after-potential which reaches the threshold membrane potential to initiate repetitive after-discharges. We have developed the method with which the percentage of sodium channel population that needs to be modified to cause repetitive after-discharges can be measured accurately. In rat cerebellar Purkinje neurons, only 0.6% of sodium channels needs to be modified for hyperexcitation resulting in a large toxicity amplification. This concept is applicable to other neuroactive drugs that act through the threshold phenomenon. The mechanisms of selective toxicity of pyrethroids in mammals and insects have been quantitatively determined to be due mainly to the different sensitivity of the sodium channels to pyrethroids and the negative temperature dependence of pyrethroid action on the sodium channels. The degradation of pyrethroids play only a minor role. The negative temperature dependence of pyrethroid action is due to the increased sodium current flow at low temperature. The major site of action of dieldrin and hexachlorocyclohexane is the GABA(A) receptor chloride channel complex. Dieldrin exerts a dual action, initial stimulation and subsequent suppression, and the latter is responsible for hyperexcitation of animals. Dieldrin stimulation requires the gamma2s subunit in the GABA receptor, whereas dieldrin suppression occurs in the presence or absence of the gamma2s subunit.