A pharmacological analysis was made of the depolarizing acetylcholine (ACh) response found on the gastric mill 1 muscles of the crabs Cancer pagurus, Cancer irroratus and Cancer borealis.
Acetylcholine, carbamylcholine, trimethylammonium, nicotine, and dimethyl-4-phenyl-piperazinium were effective in producing contractures and depolarizations in these muscles. No response to decamethonium, suberyldicholine, acetyl-β-methylcholine, carbamyl-β-methylcholine, pilocarpine and oxotremorine could be detected.
High concentrations of muscarinic agonists (10−4 to 10−3 M) potentiated and prolonged the ACh iontophoretic response. When the acetylcholinesterase activity was inhibited with neostigmine, or when the response was elicited with carbamylcholine, muscarinic agonists partially inhibited the response.
ACh responses were most effectively blocked by vertebrate nicotinic ganglionic antagonists, including dihydro-β-erythroidine, pempidine, and mecamylamine.
α-Bungarotoxin was without effect on the ACh response.