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25 protocols using sch 23390 hydrochloride

1

Disruption of Contextual Fear Conditioning

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SCH23390 hydrochloride (0.1 mg/kg, i.p.; Tocris Bioscience, UK) was dissolved in 0.9% sterile saline. This dose has previously been shown to disrupt contextual fear conditioning (Inoue et al. 2000 (link); Heath et al. 2015 (link)). Vehicle-treated controls received injections of 0.9% sterile saline (1 mL/kg, i.p.).
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2

Electrophysiology Experiments: Pharmacological Agents

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All chemicals used for electrophysiology experiments were obtained from Sigma-Aldrich except D-L-AP5 and NBQX (from Ascent Scientific). The D1 Receptor agonist SKF 81297 hydrobromide (6-chloro-2,3,4,5-tetrahydro-1-phenyl-1H-3-benzazepine hydrobromide) and the D1R antagonist SCH 23390 hydrochloride ((R)-(+)-7chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride) were from Tocris. SKF81297 and SCH23390 were dissolved in water at a 10 mM concentration for stock solutions. Drugs were bath applied for 15 minutes before a “drug recording”.
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3

Pharmacological Modulation of Neural Signaling

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All drugs were purchased from Sigma Aldrich (St. Louis, MO), or Tocris (Bristol, UK). SKF 81297 hydrobromide (Tocris, 1447) was applied either as puff (500 µM) or flow in (10 µM) depending on experiment type. All other drugs were bath applied: SCH-39166 hydrobromide (Tocris,2299), SCH-23390 hydrochloride (Tocris, 0925), SKF-83566 hydrobromide (Tocris, 1586), Strychnine (Sigma-Aldrich, 8753), Tetraethylammonium chloride (Sigma-Aldrich, 86614), TTX (Tocris Bioscience, 1069), (RS)-CPP (Tocris Bioscience, 0173), NBQX (Tocris Bioscience, 0373), SR 95531 hydrobromide (Tocris Bioscience, 1262), MNI-caged-L-glutamate (Tocris Biosciences 1490), L-741,626 (Tocris Bioscience, 1003), Pyr-3 (Tocris,3753), prazosin (Sigma-Aldrich, P7791), propranolol (Sigma-Aldrich, 40543), and quinpirole hydrochloride (Tocris Bioscience, 1061). For experiments requiring pharmacological agents dissolved in DMSO the concentration never exceeded 0.02% DMSO.
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4

Methamphetamine-Induced Cognitive Deficits

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The drugs used were (+)-methamphetamine hydrochloride (Sigma, St Louis, MO) and SCH23390 hydrochloride (TOCRIS bioscience, Ellisville, MO). All drugs were diluted with 0.9% saline. We have selected the METH dose based on previous studies showing that repeated non-contingent 7 days METH treatment (1 mg/kg) was able to induce cognitive impairments associated with deficits of the ERK1/2 pathway in the mPFC (González et al., 2014 (link); also see Kamei et al., 2006 (link)). In the present study, METH was administered subcutaneously (s.c.) once a day for 7 days (1 mg/Kg, calculated as free base). To test D1/5 receptors effect, animals received intraperitoneal (i.p.) injections of the D1 receptor antagonist, SCH 23390 (0.5 and 0.05 mg/kg, for 7 days), 30 min before each injection of saline or METH. Vehicle groups received the same volume of sterile saline solution. Mice were killed 4 days after the last METH/saline injection.
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5

Cocaine and Dopamine Receptor Ligands

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Cocaine hydrochloride was supplied by the National Institute on Drug Abuse (National Institutes of Health, Bethesda, MD). (S)-eticlopride hydrochloride was purchased from Sigma-Aldrich (St. Louis, MO), SCH 23390 hydrochloride, from Tocris (Ellisville, MO). Cocaine and SCH 23390 were dissolved in 0.9% saline. Eticlopride was dissolved in ethanol and diluted to ≤1% ethanol in sterile water.
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6

Pharmacological Modulation of Locomotion

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The drugs used were (+)-methamphetamine hydrochloride (Sigma, St Louis, MO), SCH23390 hydrochloride (TOCRIS bioscience, Ellisville, MO), raclopride (TOCRIS bioscience, Ellisville, MO), and modafinil (racemic mixture of R- and S-enantiomers), generously donated by Laboratorios Beta S.A. (Argentina). METH, SCH23390, and raclopride were diluted with 0.9% sterile saline, and modafinil was administered as a suspension in carboximethylcellulose 0.5% in saline. In the present study, we evaluated the effect of METH (1 mg/kg, s.c.) or modafinil (90 mg/kg i.p.) as a single dose. For vehicle administration, half of the mice received saline s.c. and the other half received 0.5% carboximethylcellulose in saline. All mice were sacrificed 1 hr after METH or modafinil injection. modafinil and METH administration increased locomotion compared to vehicle (see Figure S1 in Supplemental information). In a separate groups of animals, the D1/5 receptor antagonist, SCH23390 (0.05 mg/kg i.p.) or the D2/3/4 receptor antagonist raclopride (8 mg/kg i.p.), were administered 30 min before the METH or modafinil injection. These doses were chosen based on previous studies by our laboratory using SCH23390 (González et al., 2016 (link)), and from others demonstrating that raclopride at this dosage was able to antagonize the effects of METH on an mPFC-dependent NOR task (Kamei et al., 2006 (link)).
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7

Pharmacological Modulation of Neuronal Signaling

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Picrotoxin and MK-801 were from Abcam. CGP55845, DNQX, Dihydro-β-erythroidine hydrobromide, SCH 23390 hydrochloride, and sulpiride were obtained from Tocris Bioscience. BAPTA was obtained from Invitrogen. ω-Conotoxin GVIA and ω-Agatoxin TK were from Alomone Labs. All the other chemicals (α-methyl-DL-tyrosine, DEAB, TTX, 4-Aminopyridine, EGTA-AM, BAPTA-AM, scopolamine hydrobromide) were from Sigma-Aldrich.
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8

Nicotine self-administration and dopamine receptor modulation

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(−)-Nicotine hydrogen tartrate (Sigma-Aldrich), SCH 23390 hydrochloride (Tocris bioscience), and A77636 hydrochloride (Tocris bioscience) were dissolved in sterile saline (0.9% sodium chloride). SCH 23390 and A77636 were administered subcutaneously (SC) in a volume of 1 ml/kg body weight. Nicotine was dissolved in sterile saline, and the rats self-administered 0.03 or 0.06 mg/kg/inf of nicotine in a volume of 0.1 ml/inf. Nicotine doses are expressed as base, and SCH 23390 and A77636 doses are expressed as salt. The treatment schedule was the same in experiments 1–3. Both SCH 23390 and A77636 were administered (SC) 15 min before nicotine self-administration, food responding, or the small open field test. It was also determined if SCH 23390 affected nicotine and food intake and locomotor activity 24 h after treatment and if A77636 affected these parameters 24 and 48 h after treatment. The doses of SCH 23390 and A77636 were based on previous studies in rats18 (link),61 (link). SCH 23390 (0, 0.003, 0.01, and 0.03 mg/kg), and A77636 (0, 0.1, and 0.3 mg/kg) were administered according to a Latin square design. The highest dose of A77636, 1 mg/kg, was not included in the Latin square design and was administered last. There was at least 48 h between injections with SCH 23390 and 72 h between injections with A7763661 (link).
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9

CAMP Signaling Pathway Modulation

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8-(4-chlorophenylthio) adenosine-3’,5’-cyclic monophosphate (8-CPT-cAMP) was purchased from BIOLOG Life Science Institute. The inhibitors 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ22536), 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene (U0126), N-[2-[[3-(4-bromophenyl)-2-propenyl-]amino]ethyl]-5-isoquinolinesulfonamide dihydrochloride (H-89), and α-[amino[(4-aminophenyl)thio]methylene]-2-(trifluoromethyl)benzeneacetonitrile (SL327), and D1 receptor ligands SKF81297 hydrobromide and SCH-23390 hydrochloride were purchased from Tocris. Reserpine and phorbol 12-myristate 13-acetate (PMA) were obtained from Sigma. Drug stocks were prepared at 50 or 100 mM in DMSO, followed by dilution in culture media to final concentrations of 100 μM 8-CPT-cAMP, 10 μM Reserpine, 10 μM U0126, 30 µM H89, 1 mM SQ22536, 10 µM SCH-23390, 10 µM SKF 81297, and 100 nM PMA.
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10

Acute Pharmacological Manipulation of Dopaminergic System in Mice

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Three-month-old PERKf/f DAT-Cre and WT DAT-Cre mice were acutely administered i.p. with the DAT inhibitor GBR-12783 dihydrochloride (Tocris Bioscience, cat no: 0421) at a doses of 6 or 10 mg/kg, the VMAT2 inhibitor reserpine (Tocris Bioscience, cat no: 2742) at a dose of 1 or 1.5 mg/kg, or the D1 receptor antagonist SCH 23390 hydrochloride (Tocris Bioscience, cat no: 0925) at a dose of 0.01 or 0.2 mg/kg, and motor activity was assessed using the drag, the rotarod, and the open field tests. Mice were tested 20 min (GBR-12783; SCH 23390) or 24 hr (reserpine) after drug administration. Experimenters were blind to the genotype and treatment.
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