作者: Churl K. Min , Gregory A. Weiland
DOI: 10.1016/0006-8993(92)91647-W
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摘要: The effect of substance P on nicotinic acetylcholine receptor function was examined in Torpedo electroplaque membranes. peptide inhibited carbamylcholine-stimulated 22Na+ efflux a concentration-dependent manner. By irreversibly blocking spare receptors with alpha-bungarotoxin, the IC50 for shown to be less than 3 microM. Inhibition by slow relative activation carbamylcholine, consistent an enhancement desensitization or allosteric block.