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Cgp55845

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CGP55845 is a laboratory product manufactured by Merck Group. It is a compound used for research purposes. No further details about its core function or intended use are provided, as an unbiased and factual description must be maintained.

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Lab products found in correlation

Gabazine, by Merck Group (3 mentions) Picrotoxin, by Merck Group (2 mentions) Sulpiride, by Merck Group (2 mentions) Baclofen, by Merck Group (2 mentions) Bicuculline, by Merck Group (2 mentions) Dmso dimethyl sulfoxide, by Merck Group (1 mentions) Am251, by Merck Group (1 mentions) Dopamine hydrochloride, by Merck Group (1 mentions) Nifedipine, by Merck Group (1 mentions) Sch58261, by Bio-Techne (1 mentions) D apv, by Bio-Techne (1 mentions) Bapta tetrapotassium salt, by Thermo Fisher Scientific (1 mentions) Strychnine, by Merck Group (1 mentions) Coelenterazine ctz, by Nanolight Technology (1 mentions) Chloral hydrate, by Sinopharm (1 mentions) Ab81213, by Abcam (1 mentions) Ab55051, by Abcam (1 mentions) Quinpirole, by Merck Group (1 mentions) Isoflurane, by Performance Health (1 mentions) Gabaculine, by Enzo Life Sciences (1 mentions)

12 protocols using cgp55845

1

Microinjection of CB1 and GABA-B Antagonists in Dentate Gyrus

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We used the 4-methyl-1-H-pyrasole- 3-carboxamide (AM251) as a synthetic CB1 receptor antagonist prepared from Sigma, USA and the GABAB receptor antagonist (2S)-3-[[(1S)-1-(3,4-dichlorophenyl) ethyl]amino-2-hydroxypropyl](phenylmethyl) phosphinic acid hydrochloride (CGP55845; Sigma, USA). CGP55845 and AM251 were first dissolved in DMSO (dimethylsulfoxide) (Sigma, USA), followed by diluting in saline (0.9% NaCl). The concentration of DMSO was < 10%. DMSO and saline were applied as the vehicle. Microinjection of the drugs into the DG was done through a 27-gauge stainless steel injector that was attached to Hamilton microsyringe (1 µl) by PE-20 tubing about 20 min before HFS. Therefore, 0.5 µl of the drugs was microinjected unilaterally using a microsyringe pump and Hamilton syringes at 0.5 µl/min for 1 min. After combination of the drugs, their amount was twice and their final amount was the same (0.5 µl). We left the injection syringe in position for 60 s prior to withdrawal for minimizing dragging of the administrated solutions along the injection tract. The used solutions were prepared promptly before their usage. The concentrations of the drugs was according to earlier investigations: AM251: 0/1 µg/rat [28 (link), 32 (link), 33 (link)], and CGP55845: 1 µg/rat [28 (link), 34 (link)].
Nazari M., Karimi S.A., Komaki S., Kourosh Arami M, & Komaki A. (2023). Underlying mechanisms of long-term potentiation during the inhibition of the cannabinoid CB1 and GABAB receptors in the dentate gyrus of hippocampus. BMC Neuroscience, 24, 3.
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2

Electrophysiological Recording in Neurons

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Reagents used for aCSF, the internal pipette solution, dopamine hydrochloride, sulpiride, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), APV, CGP-55845, and picrotoxin (PTX) were purchased from Sigma-Aldrich (Oakville, ON, Canada). All drugs were prepared fresh by dissolving them in distilled water.
Darvish-Ghane S., Baumbach J, & Martin L.J. (2023). Influence of Inflammatory Pain and Dopamine on Synaptic Transmission in the Mouse ACC. International Journal of Molecular Sciences, 24(13), 11113.
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3

Receptor Blockade in Electrophysiology

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Where applicable, CGP 55845 (2 µM; Sigma-Aldrich, Germany), DPCPX (100 nM; Biotrend) or SCH 58261 (50 nM, Tocris Cookson, Bristol, UK) was bath perfused to selectively block GABAB, A1 or A2A receptors, respectively. Bath perfusion of NBQX (10 μM; Biotrend, Germany), D-APV (50 µM; Tocris Cookson, Bristol, UK) or S-MCPG (500 μM; Biotrend) was used to block AMPARs, NMDARs or metabotropic GluRs, respectively. Nifedipine (10 µM; Sigma-Aldrich, Germany) was used to block L-type voltage-gated Ca2+ channels.
Berberich S., Pohle J., Pollard M., Barroso-Flores J, & Köhr G. (2017). Interplay between global and pathway-specific synaptic plasticity in CA1 pyramidal cells. Scientific Reports, 7, 17040.
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4

Studying Neuronal Synaptic Transmission

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The normal aCSF comprised (in mM) 124 NaCl, 3.5 KCl, 1 MgCl2, 1.6 CaCl2, 26 NaHCO3, 1.25 NaH2PO4 and 10 glucose (pH 7.35; osmolarity 305 mOsm) to which 6‐cyano‐7‐nitro‐quinoxaline‐2,3‐dione (CNQX; 15 µM), 2‐amino‐5‐phosphono‐valeric acid (D‐APV; 50 µM), Picrotoxin (100 µM) and 3‐Aminopropyl)(diethoxymethyl) phosphinic acid hydrate (CGP‐55845; 1 μM) were added to block synaptic transmission. We used 1.6 mM CaCl2 in the aCSF because in bicarbonate buffer system this concentration yields 1.2 mM free Ca2+, corresponding to the baseline interstitial brain Ca2+ concentration measured in vivo (e.g., Jones & Keep, 1988). In most experiments, as indicated, the aCSFs contained also the HCN channel blocker 4‐4thylphenylamino‐1,2‐dimethyl‐6‐methylamino‐pyrimidinium chloride (ZD7288; 50 μM). The ACSFs designed to block voltage‐gated Ca2+ channels contained also NiCl2 (200 µM) and CdCl2 (200 µM). In K+‐free aCSF KCl was omitted. Picrotoxin, CGP‐55845, NiCl2, CdCl2 and ouabain were obtained from Sigma‐Aldrich Ltd. (Rehovot, Israel), CNQX and APV from Alomone Labs (Jerusalem, Israel), ZD7288 and XE991 from Tocris Bioscience (Bristol, UK), and BAPTA tetra‐potassium salt from Thermo Fisher Scientific (Waltham, MA).
Tiwari M.N., Mohan S., Biala Y, & Yaari Y. (2018). Differential contributions of Ca2+‐activated K+ channels and Na+/K+‐ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells. Hippocampus, 28(5), 338-357.
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5

Bioluminescent Neuronal Signaling Assay

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The luciferase substrate, coelenterazine (CTZ), was purchased from NanoLight Technology (Pinetop, AZ): Coelenterazine free base, the natural form of CTZ (NanoLight # 303), was dissolved at 50 mM in NanoFuel (NanoLight # 399); CTZ was further diluted 1:50 in culture medium for a 1 mM working solution that was further diluted 1:100 when added to MEAs for a final concentration of 10 μM. The same dilutions were carried out with just NanoFuel for vehicle. Cocktail of synaptic blockers included NBQX (abcam # ab120046), D-AP5 (abcam # ab120003), Gabazine (Sigma Aldrich # S106), CGP 55845 (Sigma Aldrich # SML0594) and Strychnine (Sigma Aldrich # S0532). Botulinum Neurotoxin (BoNT/A1) was purchased from Metabiologics (Madison, Wisconsin).
Prakash M., Murphy J., St Laurent R., Friedman N., Crespo E.L., Bjorefeldt A., Pal A., Bhagat Y., Kauer J.A., Shaner N.C., Lipscombe D., Moore C.I, & Hochgeschwender U. (2022). Selective control of synaptically-connected circuit elements by all-optical synapses. Communications Biology, 5, 33.
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6

GABA Receptor Pharmacology and Immunohistochemistry

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Chloral hydrate was purchased from Sinopharm Chemical Reagent Co (Shanghai, China). IBO (dissolved in PBS, 5 μg/μl). Gabazine (S106, GABA-A receptor antagonist, diluted in DMSO, 1 M), and CGP55845 (SML0594, GABA-B receptor antagonist, diluted in DMSO, 1 M) were purchased from Sigma-Aldrich Co (St. Louis, MO). Anti-GABA-A receptor alpha 1 (ab94585, mouse-origin monoclonal antibody, 1:200), anti-GABA-B receptor 1 (ab55051, mouse-origin monoclonal antibody, 1:200), and anti-Brn3a antibody (ab81213, rabbit-origin monoclonal antibody, 1:200) were obtained from Abcam (Cambridge, MA).
Gong J.L., Lou X.T., Yuan Y.X., Chen L.W., Ji P.T., Li L., Zhao Y, & Zhang H. (2018). The increased expression of GABA receptors within the arcuate nucleus is associated with high intraocular pressure. Molecular Vision, 24, 574-586.
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7

Striatal Slice Voltammetry in Mice

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Isoflurane (Patterson Veterinary, Devens, MA) anesthetized mice were sacrificed by decapitation and brains were rapidly removed, sectioned into thick coronal striatal slices (300–400μm; Leica VT1000S, Vashaw Scientific, Norcross, GA), incubated for 60 minutes at 34 °C in pre-oxygenated (95% O2/5% CO2) artificial cerebral spinal fluid (aCSF). The aCSF consisted of (in mM): NaCl (126), KCl (2.5), NaH2PO4 (1.2), MgCl2 (1.2), NaHCO3 (25), D-glucose (11), L-ascorbic acid (0.4), with pH adjusted to ~7.4. Cutting solution also contained either MK801 (10 μM; (5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine; Abcam, Cambridge, UK) or kynurenic acid (2 mM) for blockade of ionotropic glutamate receptors. At the end of the incubation period, tissue was transferred to aCSF (34 °C) without glutamate receptor blockers. The following concentrations of drugs were bath applied for slice voltammetry experiments where specified: Baclofen (30 μM), CGP55845 (200 nM), quinpirole (10 μM), sulpiride (600 nM; Sigma), 2β-propanoyl-3β-(2-naphthyl)-tropane (WF-23) (10 nM – 3 μM; Huw M. L. Davies, Emory University, Atlanta DA), 2β-propanoyl-3β -(4-tolyl)-tropane (PTT) (100 nM – 30 μM; Huw M. L. Davies), cocaine (300 nM - 30 μM; NIDA, Rockville, MD USA).
Everett A.C., Graul B.E., Ronström J.W., Robinson J.K., Watts D.B., España R.A., Siciliano C.A, & Yorgason J.T. (2022). Effectiveness and relationship between biased and unbiased measures of dopamine release and clearance. ACS chemical neuroscience, 13(10), 1534-1548.
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8

Intrathecal GABA Modulators for Spinal Protection

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GABA receptor antagonists and GABA transaminase inhibitor were delivered via an intrathecal catheter placed at thoracic T1 to T4 spinal level inserted through a small incision in dura mater at thoracic spinal level 5. The lowest therapeutic dose was chosen based on literatures30 (link)–33 (link). For the GABAA/B receptor antagonists 1000 microgram of GABAA antagonist Bicuculline (Sigma-Aldrich) or 3000 microgram of GABAB antagonist CGP55845 (Sigma-Aldrich) were dissolved in 2 milliliters of normal saline and warmed to 37° Celsius, were infused over 5 minutes using a syringe pump. Given that the peak dorsal horn drug concentration occurs 30 minutes after intrathecal administrations, each antagonist was applied 30 minutes before starting Ischemia/reperfusion and reapplied at 60 minute intervals. GABA transaminase inhibitor, GABAculine, was used as inhibition of GABA transaminase reduces the degradation of GABA leading to increased neuronal GABA concentrations34 (link). 5 milligrams of GABAculine (Enzo) was dissolved in 1milliliter DMSO and 4 milliliter saline, 2 milligrams GABAculine was infused over 5 minutes using a syringe pump, 30 minutes prior to Ischemia/reperfusion, with no spinal cord stimulation, and reapplied at 60 minutes interval.
Howard-Quijano K., Kuwabara Y., Yamaguchi T., Roman K., Salavatian S., Taylor B, & Mahajan A. (2023). GABAergic Signaling During Spinal Cord Stimulation Reduces Cardiac Arrhythmias in a Porcine Model. Anesthesiology, 138(4), 372-387.
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9

Pharmacological Manipulation of Synaptic Transmission

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MK-801 (10 μM), an uncompetitive NMDAR antagonist, QX314 (6 µM), voltage-gated Na+ channel blocker, bicuculline (10 µM), a competitive GABAa receptor antagonist, CGP 55845, a selective GABAb receptor antagonist (5 µM), and DNQX (20 µM), a competitive AMPA and kainate receptor antagonist, were obtained from Sigma (St. Louis, MO, USA). These drugs, used for the electrophysiology experiments, were diluted in distilled water and applied via a bath.
Postnikova T.Y., Malkin S.L., Zakharova M.V., Smolensky I.V., Zubareva O.E, & Zaitsev A.V. (2021). Ceftriaxone Treatment Weakens Long-Term Synaptic Potentiation in the Hippocampus of Young Rats. International Journal of Molecular Sciences, 22(16), 8417.
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10

Compound E139 Synthesis and Application

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Compound E139 was synthesized in house [11 (link)]; stock solutions were prepared in dimethyl sulfoxide (Sigma; St. Louis, Mo., USA), aliquoted into 40-μl portions, stored at −20°C, and used within 2 weeks. Paclitaxel and GABA were purchased from Tocris (Bristol, UK), CNQX from Tocris (Ellisville, Mo., USA); ethanol, Cremophor EL, CGP 55845, the salts used in the preparation of artificial cerebrospinal fluid (aCSF), and recording solutions were from Sigma (St. Louis, Mo., USA). All stock solutions were diluted to the desired concentrations with aCSF before use and applied to the tissue slices by bath perfusion.
Nashawi H., Masocha W., Edafiogho I.O, & Kombian S.B. (2016). Paclitaxel Causes Electrophysiological Changes in the Anterior Cingulate Cortex via Modulation of the γ-Aminobutyric Acid-ergic System. Medical Principles and Practice, 25(5), 423-428.
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