[3H]cocaine binding in brain is inhibited by tris (hydroxymethyl) aminomethane

Reith, Maarten E. A.; Meisler, Bernard E.; Sershen, Henry; Lajtha, Ábel

doi:10.1016/0165-0270(84)90014-1

Cited by 17 publications

(11 citation statements)

References 4 publications

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“…Although Tris decreases total DAT binding (Reith et al, 1984) Little et al, 1999). Dopamine uptake affinity in the hDAT-N2A cells has varied in the 200 to 500 nM range in our laboratory over a period of several years, and the range of [ 3 H]dopamine Although a comparison of dose concentrations and time scales between cells in culture and living animals or humans is inexact, the present results parallel animal experiments finding that relatively large cumulative doses of cocaine (generally more than 200 mg/kg/rat) are required to consistently cause DAT up-regulation (Alburges et al, 1993;Koff et al, 1994;Wilson et al, 1994;Hitri et al, 1996;Letchworth et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Because a Tris buffer has been used to assess cocaine effects on DAT regulation in the past (Little et al, 1993(Little et al, , 1999, and the inclusion of Tris in assay buffer has been found to decrease absolute B max for DAT binding sites (Reith et al, 1984), experiments were performed examining the effect of cocaine exposure on DAT binding in an assay buffer containing 50 mM Tris/120 mM NaCl, instead of the phosphate/sucrose buffer. In these experiments (n ϭ 3), [ Effects of Cocaine Treatment on Total DAT Concentrations, DAT mRNA, and Subcellular Location.…”

Section: Effects Of Cocainementioning

confidence: 99%

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Cocaine Induction of Dopamine Transporter Trafficking to the Plasma Membrane

Little

Elmer²,

Zhong³

et al. 2002

Mol Pharmacol

139

107

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Little et al., 1993Little et al., , 1999Staley et al., 1994), accompanied by up-regulation of dopamine uptake (Mash et al., 1997). Such functional alterations could be important, perhaps contributing to cocaine-induced binging, withdrawal symptoms, or craving. Beyond drug self-administration, dopamine neurons play a role in other rewarding phenomena, including sex (Everitt, 1990) and eating (Phillips et al., 1993), suggesting that regulatory alterations in DAT function could have interesting implications for understanding the dynamics of a number of motivational and appetitive processes. Recent experiments in cell culture have determined that phosphorylative treatments (Pristupa et al., 1998;Daniels et al., 1999;Melikian and Buckley, 1999) or exposure to the stimulant d-amphetamine (Saunders et al., 2000) dynamically regulate DAT function by changing DAT cellular localization, perhaps invoking mechanisms that might be related to those activated by cocaine.Understanding the mechanisms involved in DAT binding site changes is important because 1) binding site alterations are the primary alterations documented in postmortem brain from cocaine users; 2) DAT inhibitors/ligands are being developed extensively as both therapeutic and imaging agents for both the DAT as well as dopamine neurons; and 3) DAT regulation may provide broader insights into the pharmacological effects of drugs on transporter binding sites. In addition to our need to uncover cocaine's neurochemical effects that provoke symptoms associated with its dependence, it is possible that new therapeutic or imaging agents (many of which are often DAT uptake inhibitors) might themselves induce adaptations in DAT function, as well as alter cocaine's effect on dopamine uptake. Also, potentially, DAT inhibitor binding sites could be altered through some mechanism that is independent of changes in DAT concentration or function.

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Section: Discussionmentioning

confidence: 99%

Section: Effects Of Cocainementioning

confidence: 99%

Cocaine Induction of Dopamine Transporter Trafficking to the Plasma Membrane

Little

Elmer²,

Zhong³

et al. 2002

Mol Pharmacol

139

107

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“…Caudates were dissected 60 min after the injection, and striatal membranes were prepared as described in section 2. As shown in fig.1, this dose of GBR12909 produced a To label 13H]cocaine binding sites [19], striatal membranes were incubated in 12 x 75 mm polystyrene test tubes for 20-60 min at 0°C (equilibrium) in 25 mM sodium phosphate buffer, pH 7.4, with 10 nM ['HIcocaine (spec. act.…”

Section: Lrgand Binding Assaysmentioning

confidence: 99%

Tight binding dopamine reuptake inhibitors as cocaine antagonists

Rothman¹,

Mele²,

Reid³

et al. 1989

FEBS Letters

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The experiments reported in this study tested the hypothesis that tight binding dopamine (DA) reuptake inhibitors might act as cocaine antagonists. Binding studies demonstrated that the high affinity dopamine reuptake inhibitor, I-[2-[bis(efluorophenyl)methoxy]ethyl]-4_raz-ine (GBR12909) produced a wash-resistant inhibition of the DA transporter in rat striatal membranes as labeled by PHIcocaine or PH]l-[2-(diphenyl-methoxy)ethyl]-4-(3-phenylpropyl)piperazine(PH]GBR12935), indicative of tight binding. In vivo microdialysis experiments showed that administration of 25 mg/kg GBR12909 to rats produced a modest, but not statistically significant, increase in the extracellular levels of striatal DA, while this same dose of GBR12909 inhibited the ability of cocaine to elevate extracellular DA levels by 64%. These data suggest that tight binding DA reuptake blockers may provide a fruitful approach for developing a cocaine antagonist.Cocaine; Dopamine reuptake inhibitor; Microdialysis, in vivo; Dopamine

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“…higher affinity for cocaine) were reported when binding was measured in 0.32 M sucrose buffered with 10 mM Na,HPO, (9, lo), compared with values obtained using 50 mM Tris, 120 mM NaCl (20,26,39). Reith and co-workers (32) were the first to observe that binding of ['Hlcocaine was much lower if measured in Tris buffer. We confirmed that effect and reported a dose-dependent inhibition of [3H]cocaine binding to striatal membranes by Tris.…”

Section: Introductionmentioning

confidence: 97%

“…The binding of [3H]cocaine has been used to identify cocaine receptors in the mammalian brain (5,9,10,20,26,32,39). However, neither the assay conditions nor buffers have been standardized.…”

Section: Introductionmentioning

confidence: 99%

Allosteric Regulation by Sodium of the Binding of [³H]Cocaine and [³H]GBR 12935 to Rat and Bovine Striata

Eshleman

Calligaro²,

Eldefrawi

1993

Membrane Biochemistry

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Sodium regulation of ligand binding to the dopamine transporter of rat and/or bovine striata was investigated using a filtration binding assay. In low Na+ phosphate or bicarbonate-buffered sucrose (300 mOsm), the tissue exhibited high affinity for [3H]cocaine which was reduced by the addition of Na+ in a dose-dependent manner. However, [3H]GBR 12935 binding was insensitive to Na+ in these physiological buffers. Although binding of [3H]GBR 12935 was displaced by cocaine in a manner consistent with competitive displacement, a non-linear affinity shift of the displacement of [3H]GBR 12935 by cocaine suggests that the two ligands bind to distinct sites. Binding of both radioligands was suppressed when measured in sodium-free 50 nM Tris-sucrose and increased with the addition of Na+. Scatchard analysis indicated that Bmax for [3H]cocaine binding in Tris plus 120 mM NaCl reached the same level as in the physiological buffers. In Krebs-Ringer buffer with phosphate, bicarbonate or Tris, which contained 120 nM NaCl, both [3H]cocaine and [3H]WIN 35428 binding exhibited lower affinities than in Na(+)-deficient phosphate buffer. It is suggested that the cation form of Tris binds to the dopamine transporter and that the Tris-receptor complex does not bind [3H]cocaine or [3H]GBR 12935. Na+ displaces Tris, forming a Na(+)-receptor complex which binds these ligands. Thus, it is suggested that the Na(+)-dependent binding of cocaine to the dopamine transporter is observed only in Tris.

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[3H]cocaine binding in brain is inhibited by tris (hydroxymethyl) aminomethane

Cited by 17 publications

References 4 publications

Cocaine Induction of Dopamine Transporter Trafficking to the Plasma Membrane

Cocaine Induction of Dopamine Transporter Trafficking to the Plasma Membrane

Tight binding dopamine reuptake inhibitors as cocaine antagonists

Allosteric Regulation by Sodium of the Binding of [³H]Cocaine and [³H]GBR 12935 to Rat and Bovine Striata

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[3H]cocaine binding in brain is inhibited by tris (hydroxymethyl) aminomethane

Cited by 17 publications

References 4 publications

Cocaine Induction of Dopamine Transporter Trafficking to the Plasma Membrane

Cocaine Induction of Dopamine Transporter Trafficking to the Plasma Membrane

Tight binding dopamine reuptake inhibitors as cocaine antagonists

Allosteric Regulation by Sodium of the Binding of [3H]Cocaine and [3H]GBR 12935 to Rat and Bovine Striata

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Allosteric Regulation by Sodium of the Binding of [³H]Cocaine and [³H]GBR 12935 to Rat and Bovine Striata