The effects of avermectin and drugs related to acetylcholine and 4-aminobutyric acid on neurotransmission in Ascaris suum

We have examined some aspects of the neuropharmacology of the nematode Ascaris suum using a divided chamber and selective stimulation techniques to localize the sites of action of drugs. These techniques enabled us to investigate separately excitatory neuromuscular transmission, inhibitory neuromuscular transmission, and transmission from interneurons to excitatory motorneurons. We find that a curare-sensitive mechanism is involved in the excitation of the excitatory motorneuron via interneurons. The anthelmintic avermectin B_1a (AVM) also blocks interneuronal stimulation of excitatory motorneurons. This action of AVM can be reversed by picrotoxin. AVM has no effect on excitatory neuromuscular transmission. Two GABAergic agonists in nematodes, muscimol and piperazine, mimic the effects of AVM when applied ventrally. This suggests that the action of AVM is related to a GABAergic mechanism. Ventral inhibitory neuromuscular transmission is also blocked by AVM, but this action is not reversed by picrotoxin. Thus AVM has two distinct sites of action in A. suum.