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However, despite the physiological characterization of mouse models and cell lines, the precise pathophysiology of nAChRs outside the CNS remains not well understood, in part because there is a lack of subtype\u2010selective antagonists. \u03b1\u2010Conotoxins isolated from cone snail venom exhibit characteristic individual selectivity profiles for nAChRs and, therefore, are excellent tools to study the determinants for nAChR\u2010antagonist interactions. Given that human \u03b13\u03b24 subtype selective \u03b1\u2010conotoxins are scarce and this is a major nAChR subtype in the PNS, the design of new peptides targeting this nAChR subtype is desirable. Recent studies using \u03b1\u2010conotoxins RegIIA and AuIB, in combination with nAChR site\u2010directed mutagenesis and computational modelling, have shed light onto specific nAChR residues, which determine the selectivity of the \u03b1\u2010conotoxins for the human \u03b13\u03b22 and \u03b13\u03b24 subtypes. Publications describing the selectivity profile and binding sites of other \u03b1\u2010conotoxins confirm that subtype\u2010selective nAChR antagonists often work through common mechanisms by interacting with the same structural components and sites on the receptor.<\/jats:p><\/jats:sec><jats:sec><jats:title>Linked Articles<\/jats:title><jats:p>This article is part of a themed section on Nicotinic Acetylcholine Receptors. 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