Differentiation of Acetylcholine and Succinylcholine Receptors in Leech Muscle

Abstract

In a study on the effects of some agonists on the leech muscle, Flacke & Yeoh (1968) showed that two groups of agonists, acetylcholine, carbachol and nicotine on the one hand, and succinyicholine and decamethonium on the other, could be differentiated by their potencies and the sizes of the maximal responses obtainable. It was thought that these differences could be explained on the basis of different sites of action of the two groups of agonists. This possibility was tested, and the present communication describes the interaction of the two groups of agonists with each other and with antagonist agents. METHODSThe methods used have already been described (Flacke & Yeoh, 1968). The effects of different concentrations of an antagonist agent were determined after exposure of at least 30 min to each concentration. The antagonist was present throughout the test sequence-that is, during and between successive tests with an agonist. Exposure to the agonist was for a period of 30 sec. The shift in the concentration-response curves was determined with concentrations of the agonist causing 20-80% of the estimated maximum response, which was determined only at the end of the experiment by adding a supramaximal dose; this procedure was necessary because a maximum response was followed by a period of depressed sensitivity. The effect of an antagonist was measured by determining the concentration ratio of the agonist at 50% of the maximum response. DrugsThe following drugs were used: acetylcholine chloride (Merck); carbaminoylcholine chloride (Merck); nicotine hydrogen tartrate (BDH); succinylcholine chloride (Burroughs Wellcome); decamethonium bromide (Burroughs Wellcome); physostigmine sulphate (Merck); (+)-tubocurarine chloride (Abbott); gallamine triethiodide (Davis and Greck). All drug concentrations are expressed as molar concentrations of the base. RESULTSPreliminary experiments confirmed earlier observations by several investigators (Minz,

A Note on the Effect of Dithiothreitol (Dtt) on the Depolarization of Isolated Sympathetic Ganglia by Carbachol and Bromo‐acetylcholine

“…Karlin & Winnik, 1968;Rang & Ritter, 1971). This suggests a closer resemblance of the ganglionic nicotinic receptor to that for mono-quaternary nicotinic agonists in leech dorsal muscle (Flacke & Yeoh, 1968;Ross & Triggle, 1972). This analogy is strengthened by observations that a-bungarotoxin is ineffective on both carbachol receptors in leech muscle (Ross & Triggle, 1972) and on ganglionic nicotinic receptors (Magazanik, Ivanov & Lukomskaya, 1974;D.A.…”

Receptor Mechanisms Fourth Gaddum Memorial Lecture, School of Pharmacy, University of London, January 1973

“…Studies with other substances that cause contraction of the muscle, such as potassium ions or caffeine, showed that the effect was specific to cholinergic receptors. Moreover, in leech muscle, where there are separate receptors for agents such as carbachol and acetylcholine on the one hand, and for suxamethonium and decamethonium on the other (Flacke & Yeoh, 1968a), the enhancement of desensitization by DPC1o affected only the suxamethonium receptors. Flacke & Yeoh (1968b) found that tubocurarine itself acted in the same way when tested against suxamethonium in leech muscle, but not when tested against carbachol.…”