Many hymenopteran insects incapacitate their prey by means of a neurotoxin. The glutamatergic excitatory neuromuscular transmission and the nicotinic excitatory synaptic transmission of insects is reversibly blocked by philanthotoxins, as well as by structurally related polyamine toxins isolated from spider venoms. These polyamine toxins are cation channel blockers or change at least the glutamatergic channel kinetics. They therefore are not receptor specific and are, for example, also active at the nicotinic receptors in the insect brain, albeit at higher concentrations. Poneratoxin, a 25 amino acid residue polypeptide isolated from an ant venom, is the first described hymenopteran neurotoxin affecting excitability of nerve and muscle fibres by changing the kinetics of the voltage-dependent sodium channel. The nicotinic synaptic transmission in the insect central nervous system (CNS) is presynaptically and irreversibly blocked by kinins, which probably cause transmitter depletion. Besides this delayed effect the carbohydrate-containing vespulakinins also show a direct and reversible inhibition of the synaptic transmission. Criticism on the possibilities to use venom toxins as leads in pesticide science has been, that these compounds have to be injected into the body or the CNS. For primary synthesis products the incorporation of the genetic codes into entomophilic viruses could solve this problem.Several groups of hymenopteran insects, like wasps and ants, sting their prey to a paralysis or only to a behaviourial inactivation, in order to offer the prey to the own offspring as an incapacitated, but living fresh source of food. These insects have developed venoms containing natural insecticides. The ideas of the 1980 f s included the possibility of using natural neurotoxins from arthropods as leads to new pesticides (4,(41)(42)(43).