1. Acetylcholine (ACh) elicited depolarization and an increase in input conductance of the somatic muscle cells of the parasitic nematode Ascaris suum.

  2. The relative potency of nicotinic and muscarinic agents was studied in this preparation. The order of potency of these compounds was metahydroxy phenylpropyltrimethylammonium (HPPT) > 1,1 dimethyl–4-phenylpiperazinium (DMPP) > ACh> carbachol> nicotine> tetramethylammonium (TMA+)> muscarone> furtrethonium> arecoline. Decamethonium was also a weak agonist. McN-A-343 elicited a very weak depolarization at concentrations above 1 mmol 1−1. Bethanechol and methacholine were without effect up to 1 mmol 1−1. Pilocarpine and muscarine elicited a slight hyperpolarization of up to 3 mV with a threshold for the response of around 500 μmol 1−1. Oxotremorine (1 mmol 1−1) was without effect.

  3. The nitromethylene insecticide 2(nitromethylene)tetrahydro 1,3-thiazine (NMTHT), an agonist at insect nicotinic receptors, was without effect on Ascaris muscle cells up to 1 mmol 1−1.

  4. Mecamylamine and benzoquinonium were the most potent antagonists of the acetylcholine response. The order of potency of the other antagonists was tetraphenylphosphonium (TPP) > quinacrine > pancuronium, curare > trimethaphan > atropine > chlorisondamine, Decamethonium > hexaméthonium > dihydro-β-ery throidine.

  5. The agonist profile of the Ascaris muscle cell ACh receptor clearly indicates that it is nicotinic. The potency of ganglionic and neuromuscular nicotinic receptor antagonists in Ascaris does not enable a further subclassification of this nicotinic receptor. The Ascaris nicotinic receptor seems to possess some of the pharmacological properties of each type of vertebrate nicotinic receptor. The pharmacology of the Ascaris nicotinic receptor is discussed in relation to that of nicotinic receptors in other invertebrate preparations and in vertebrate preparations.

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