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Binding was enhanced at low concentrations of HgCl<jats:sub>2<\/jats:sub>, reaching a maximum of 62% above control values at 2.5 \u03bc HgCl<jats:sub>2<\/jats:sub>. It was inhibited in a dose\u2010dependent manner at concentrations greater than 5 \u03bc HgC1<jats:sub>2<\/jats:sub>, with an IC<jats:sub>50<\/jats:sub> of 7.2 \u03bc. The increase in binding observed at the low concentrations of HgC1<jats:sub>2<\/jats:sub> was shown by Scatchard analysis to be due to an increase in the affinity of [<jats:sup>3<\/jats:sup>H]methylphenidate for its binding site on the dopamine transporter, while a decrease in both affinity and B<jats:sub>max<\/jats:sub> accompanied the reduction of [<jats:sup>3<\/jats:sup>H]methylphenidate binding observed at the higher concentrations of the inorganic mercury compound. The sodium salt of the organic mercurial <jats:italic>p<\/jats:italic>\u2010chloromercuriphenylsulfonic acid also caused an increase in [<jats:sup>3<\/jats:sup>H]methylphenidate binding (159% above controls at 2,000 \u03bc), followed by an immediate decrease in binding at higher concentrations of the reagent. Because both of these mercury\u2010containing compounds have a high propensity for interacting with sulfhydryl groups, these data suggest that the cysteine residues in the dopamine transporter molecule may play an important role in the regulation of stimulant binding to the uptake complex. \u00a9 1994 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/syn.890160304","type":"journal-article","created":{"date-parts":[[2004,12,31]],"date-time":"2004-12-31T22:20:08Z","timestamp":1104531608000},"page":"188-194","source":"Crossref","is-referenced-by-count":18,"title":["Mercuric chloride and <i>p<\/i>\u2010chloromercuriphenylsulfonate exert a biphasic effect on the binding of the stimulant [<sup>3<\/sup>H]methylphenidate to the dopamine transporter"],"prefix":"10.1002","volume":"16","author":[{"given":"M. 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