The following fluorine‐containing dopaminergic agents were used: F‐DOPA (Advanced Biochemical Compounds, Radeberg, Germany), F‐tyrosine (SynQuest, Alachua, FL, USA), F‐L‐tyrosine (Tokyo Chemical Industry, Tokyo, Japan), haloperidol (a dopamine D2 receptor antagonist; Sigma, St. Louis, MO, USA), GBR13069 dihydrochloride (GBR13069 dihydrochloride; a dopamine transporter inhibitor; Tocris, Bristol, UK), GBR12909 dihydrochloride (GBR12909; a dopamine transporter inhibitor; Tocris), 3‐bis‐(4‐fluorophenyl) methoxytropane hydrochloride (3‐bis‐FPMT; a dopamine transporter inhibitor; Tocris), flupenthixol (a non‐selective dopamine receptor antagonist; Sigma), and fenfluramine (a serotonin releaser; Sigma).
Gbr12909 dihydrochloride
Manufactured by Bio-Techne
Sourced in United Kingdom
GBR12909 dihydrochloride is a selective dopamine reuptake inhibitor. It acts by blocking the dopamine transporter, which is responsible for the reuptake of dopamine in the synaptic cleft. This product is intended for research use only and its specific applications should be evaluated by the user.
Automatically generated - may contain errors
Lab products found in correlation
3h sulpiride, by PerkinElmer (3 mentions)
Haloperidol, by Merck Group (2 mentions)
Skf38393 hydrobromide, by Bio-Techne (2 mentions)
2 cmdo, by Bio-Techne (2 mentions)
L 741 626, by Bio-Techne (2 mentions)
Atomoxetine, by Bio-Techne (2 mentions)
D amphetamine, by Bio-Techne (2 mentions)
Hydroxypropyl beta cyclodextrin, by Thermo Fisher Scientific (2 mentions)
Dopamine, by Merck Group (2 mentions)
3h 5 ht, by PerkinElmer (2 mentions)
Hek293 cell, by American Type Culture Collection (2 mentions)
Fenfluramine, by Merck Group (1 mentions)
Flupenthixol, by Merck Group (1 mentions)
Venlafaxine, by Merck Group (1 mentions)
Raclopride tartrate, by Merck Group (1 mentions)
Sch 23390 hydrochloride, by Merck Group (1 mentions)
Quinpirole dihydrochloride, by Merck Group (1 mentions)
Venlafaxine hydrochloride, by Merck Group (1 mentions)
10 protocols using gbr12909 dihydrochloride
1
Fluorine-Containing Dopaminergic Agents Protocol
2
Dopamine Modulation in Postnatal Mice
3
Selective Neuromodulator Effects on Mouse Behavior
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In all experiments mice were administered the selective COMT inhibitor tolcapone (30mg/kg; TRC Inc)(25 (link),41 (link)) and/or the selective DAT blocker GBR-12909 dihydrochloride (6mg/kg, Tocris)(42 (link)). These doses are effective at altering behavior without causing motor stereotypies (see Supplementary Information ). D-amphetamine (in sulfate formulation; Tocris) was used at 4mg/kg (43 (link)), and the NET blocker atomoxetine (in hydrochloride formulation; Tocris) at 1mg/kg (44 (link)) in the voltammetry experiment only. All drugs were dissolved in 20% hydroxypropyl-beta-cyclodextrin (Acros Organics) in 0.9% saline (AquPharm), which served as a vehicle control in all experiments. All drugs were delivered by intraperitoneal injection.
4
Selective Neuromodulator Effects on Mouse Behavior
5
Pharmacological Evaluation of Novel Dopamine and Serotonin Modulators
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GBR12909 dihydrochloride was purchased from Tocris Bioscience (Bristol, UK). Venlafaxine and dopamine were obtained from Sigma-Aldrich Chemical Co (St. Louis, MO, USA). [3H]-DA and [3H]-5-HT were purchased from PerkinElmer Life Sciences (Waltham, MA, USA). [3H]-Sulpiride (75.7 Ci/mmol) was purchased from PerkinElmer Life Sciences. The synthetic 4-benzylpiperidine carboxamides used in this study have been described in a previous study (Paudel et al., 2015 (link)). Human embryonic kidney (HEK)-293 cells were obtained from the American Type Culture Collection (Manassas, VA, USA) and maintained in minimal essential medium containing 10% fetal bovine serum, 100 U/mL penicillin, and 100 μg/mL streptomycin.
6
Pharmacological Manipulation of Behavior
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The following drugs were used: amphetamine (GlaxoSmithKline), GBR12909 dihydrochloride (Tocris), atomoxetine (Orion Pharma, capsule contents dissolved in saline followed by brief centrifugation), SCH23390 hydrochloride (Sigma), and raclopride tartrate (Sigma) were dissolved in sterile saline. All drug solutions were injected at the volume of 10 ml/kg.
7
Neurotransmitter Uptake Inhibition Assay
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GBR 12909 dihydrochloride was purchased from Tocris Bioscience (Bristol, UK). [3H]-DA and [3H]-sulpiride were purchased from PerkinElmer Life Sciences (Boston, MA, USA). Test compounds were provided by the Korean Ministry of Food and Drug Safety (Cheongju, Korea).
8
Preparation of Dopaminergic Compounds
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GBR 12909 dihydrochloride was obtained from Tocris Bioscience (Bristol, UK). R(+)-SKF 81297, (±)-quinpirole dihydrochloride and haloperidol were obtained from Sigma (St Louis, MO, USA). haloperidol was dissolved in a solution of 10% acetic acid in saline. GBR 12909, SKF 81297 and quinpirole were dissolved in saline solution.
9
Neurotransmitter Receptor Binding Assay
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GBR12909 dihydrochloride was purchased from Tocris Bioscience (Bristol, UK). Venlafaxine hydrochloride and dopamine were obtained from Sigma-Aldrich Chemical Co (St. Louis, MO, USA). [3H]-DA, [3H]-5-HT, and [3H]-sulpiride were purchased from PerkinElmer Life Sciences (Waltham, MA, USA). Human embryonic kidney (HEK)-293 cells were obtained from the American Type Culture Collection (Manassas, VA, USA) and maintained in minimal essential medium containing 10% fetal bovine serum, 100 U/mL penicillin, and 100 μg/mL streptomycin.
10
Dopamine Modulation in Postnatal Mice
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All dopamine pharmacological modulators, except for antagonists 2-CMDO (2-Chloro-11-(4-methylpiperazino)dibenz(Z)[b,f]oxepin maleate), were injected at 1 mg/kg body weight7 (link) intraperitoneally (i.p.) into nursing dams on day of birth and P2, then directly into pups until P8. 2-CMDO was injected into pups P5-P8 at 2 mg/kg body weight. Injection was done in dim red light one hour before lights on. Dopamine agonist SKF38393 hydrobromide; high affinity D2 antagonist L-741626; dopamine transporter 1 inhibitor, GBR12909 dihydrochloride; 2-CMDO were all purchased from Tocris Biosciences. For experiments with Pdgfb-icreERT2 mouse lines, 2 mg Tamoxifen was injected into nursing dams on the day of birth and on P2 to activate tamoxifen-dependent cre.
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