Ropert_1982_Neurosci_7_1963

In rats under urethane anaesthesia, various cholinomimetics, acetylcholine-antagonists and other agents were released iontophoretically in the pyramidal layer of area CA1. Like acetylcholine, a variety of cholinomimetics readily enhanced population spikes evoked by fimbrial-commissural stimulation. Judging by the equipotent iontophoretic currents, the strongest muscarinic agonist was muscarine. Other potent agonists included carbachol, methacholine, propionylcholine, bethanechol and the much slower-acting arecoline, pilocarpine and oxotremorine. Choline was about 5 times weaker than acetylcholine. Though not as effective as acetylcholine, some nicotinic agonists also consistently enhanced population spikes, particularly dimethylphenylpiperazinium and acetylthiocholine. Other nicotinic agents, such as butyrylcholine, nicotine and tetramethylammonium were much less active. Both scopolamine and atropine, given systematically in high doses (10-80 mg/kg), strongly depressed or abolished the action of muscarinic agonists, but to a lesser and more variable extent the action of ACh. They did not antagonize dimethylphenylpiperazinium. When applied iontophoretically, alpha-bungarotoxin, tubocurarine or mecamylamine did not block the action of any of the cholinomimetics. Indeed, in higher doses they tended to promote population spikes (a comparable enhancement was also seen with larger iontophoretic doses of atropine or scopolamine). On the other hand, gallamine and dihydro-beta-erythroidine antagonized muscarine but not dimethylphenylpiperazinium; a less selective block of cholinomimetics was produced by suxamethonium. It was concluded that both muscarinic and nicotinic receptors (or receptors with mixed properties) appear to be involved in the facilitatory action of acetylcholine on population spikes evoked by fimbrial-commissural stimulation.