Epibatidine dihydrochloride hydrate

Manufactured by Merck Group

Sourced in United States

Epibatidine dihydrochloride hydrate is a chemical compound used in laboratory research. It is a nicotinic acetylcholine receptor agonist. The core function of this product is to serve as a research tool for investigating nicotinic receptor activity and related biological processes.

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Lab products found in correlation

Nicotine hydrogen tartrate salt, by Merck Group (4 mentions) Cocaine hydrochloride, by Merck Group (3 mentions) Dihydro β erythroidine hydrobromide dhβe, by Bio-Techne (2 mentions) Strychnine, by Merck Group (1 mentions) Gabazine, by Bio-Techne (1 mentions) Tpmpa, by Merck Group (1 mentions) Mk 801 hydrogen maleate, by Merck Group (1 mentions) Phencyclidine hydrochloride, by Merck Group (1 mentions) Bms 933043, by Bristol-Myers Squibb (1 mentions) S ketamine hcl, by Merck Group (1 mentions)

Close spelling variants of this product

Epibatidine dihydrochloride Epibatidine

5 protocols using epibatidine dihydrochloride hydrate

Subcutaneous and Intraperitoneal Drug Assay

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The drugs were nicotine hydrogen tartrate salt (Sigma-Aldrich, St Louis, Missouri, USA), studied at pH 7, varenicline dihydrochloride (National Institute on Drug Abuse, Rockville, Maryland, USA), ± epibatidine dihydrochloride hydrate (Sigma-Aldrich), cytisine (Atomole Scientific, Hubei, China), cocaine hydrochloride (Sigma-Aldrich), and mecamylamine hydrochloride (Waterstone Technology LLC, Carmel, Indiana, USA). All drugs were administered subcutaneously except for cocaine and mecamylamine, which were administered intraperitoneal drugs were administered in a volume of saline equivalent to 10 ml/kg. Doses were expressed as their salt forms except for nicotine, which was expressed as the base weight.

de Moura F.B, & McMahon L.R. (2019). Differential cross-tolerance to the effects of nicotinic acetylcholine receptor drugs in C57BL/6J mice following chronic varenicline. Behavioural pharmacology, 30(5), 412-421.

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Perinatal Mouse Brain Manipulation

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Perinatal mice are hypothermically anesthetized for 2–3 minutes before surgery, and kept cold for the brief period during surgical injection. Pulled glass micropipettes (1B150F-4; World Precision Instruments) were loaded with AAV-Syn-GCaMP6f or AAV-Syn-jRCaMP1b and then 1–2uL was pressure injected into each ocular vitreous or transverse sinus at P0-P1. Mice are then placed on a temperature-controlled heat pad after surgery and returned to their mothers upon recovery from anesthesia. After retinal injections, we waited 4–5 days for virus to transfect and fill retinal ganglion cell axons. For acute eye injections, either (1) 0.5–1 µl of 10 µM (±)-epibatidine dihydrochloride hydrate (Sigma no. E1145) dissolved in saline, or (2) a cocktail of 1 mM AP5 (Tocris) and 200 µM NBQX (Tocris), or (3) a cocktail of 500 µM 1,2,5,6-Tetrahydropyridine-4-yl-methylphosphinic acid (TPMPA, Sigma), 50 µM gabazine (Tocris), and 5 uM strychnine (Sigma) was pressure injected using a glass micropette inserted into the vitreous.

Gribizis A., Ge X., Daigle T.L., Ackman J., Zeng H., Lee D, & Crair M.C. (2019). Visual cortex gains independence from peripheral drive before eye opening. Neuron, 104(4), 711-723.e3.

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Nicotinic Receptor Agonists and Antagonists

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The drugs included nicotine hydrogen tartrate salt (Sigma-Aldrich, St. Louis, MO), varenicline dihydrochloride (National Institute on Drug Abuse, Rockville, MD), ±epibatidine dihydrochloride hydrate (Sigma-Aldrich), cytisine (Atomole Scientific, Hubei, China), mecamylamine hydrochloride (Waterstone Technology, LLC, Carmel, IN), dihydro-β-erythroidine hydrobromide (DHβE; Tocris Biosciences, Bristol, UK), and cocaine hydrochloride (Sigma-Aldrich). Nicotine, varenicline, epibatidine, cytisine, and DHβE were administered subcutaneously. Mecamylamine and cocaine were administered intraperitoneally. All drugs were administered in a volume of saline equivalent to 10 ml/kg. Drug doses were expressed as the weight of the salt forms except for nicotine dose, which was expressed as the base weight.

de Moura F.B, & McMahon L.R. (2016). Differential Antagonism and Tolerance/Cross-Tolerance Among Nicotinic Acetylcholine Receptor Agonists: Scheduled-Controlled Responding and Hypothermia in C57BL/6J Mice. Behavioural pharmacology, 27(2-3 Spec Iss), 240-248.

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Comparative Evaluation of Nicotinic Receptor Agonists

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Drugs were nicotine hydrogen tartrate salt, with a pH adjusted to 7 (Sigma-Aldrich, St. Louis, MO), varenicline dihydrochloride (National Institute on Drug Abuse, Rockville, MD), ±epibatidine dihydrochloride hydrate (Sigma-Aldrich), cytisine (Atomole Scientific, Hubei, China), 2-fluoro-3-(4-nitro-phenyl)deschloroepibatidine (RTI-102; Dr. F. Ivy Carroll, Research Triangle Institute, NC), N-[(3R)-1-azabicyclo[2.2.2]oct-3-yl]-4-chlorobenzamide hydrochloride (PNU-282987; National Institute on Drug Abuse), ±mecamylamine hydrochloride (Waterstone Technology, LLC, Carmel, IN), dihydro-β-erythroidine hydrobromide (DHβE; Tocris Biosciences, Bristol, UK), methyllycaconitine citrate salt (MLA; National Institute on Drug Abuse), 18-methoxycoronaridine hydrochloride (18-MC; Obiter Research, Champaign, IL), midazolam hydrochloride (Ben Venue Labs, Bedford, OH), and cocaine hydrochloride (Sigma-Aldrich). Nicotine, varenicline, epibatidine, cytisine, RTI-102, midazolam, and DHβE were administered subcutaneously. PNU-282987, MLA, mecamylamine, 18-MC, and cocaine were administered intraperitoneally. All drugs were administered in a volume of saline equivalent to 10 ml/kg. Drug doses were expressed as the weight of the forms listed above except for nicotine dose, which was expressed as the base weight.

de Moura F.B, & McMahon L.R. (2016). The contribution of α4β2 and non-α4β2 nicotinic acetylcholine receptors to the discriminative stimulus effects of nicotine and varenicline in mice. Psychopharmacology, 234(5), 781-792.

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Characterization of Nicotinic and Serotonergic Receptor Cell Lines

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HEK293 cell lines expressing either the rat or human α7 nAChR (+ resistance to inhibitors of cholinesterase 3 (RIC-3)), rat α1β1δε nAChR, rat α4β2 nAChR, rat α3β4 nAChR or human 5-HT_3A receptor were developed by Bristol-Myers Squibb (Wallingford, CT, USA). The following chemicals were synthesized by Bristol-Myers Squibb: A-582941, BMS-933043, EVP-6124, NS-6740 (4-[[5-[3-(trifluoromethyl)phenyl]-2-furanyl]carbonyl]-1,4-diazabicyclo[3.2.2]nonane), PNU-282987 (N-(3R)-1-azabicyclo[2.2.2]oct-3-yl-4-chloro-benzamide hydrochloride), TC-5619, [³H]-A585539 (³H-2,2-dimethyl-5-(6-phenyl-3-pyridazinyl)-5-aza-2-azoniabicyclo[2.2.1]heptane iodide; specific activity 71 Ci/mmol, concentration 1mCi/ml). Suppliers for other reagents were as follows: (±)epibatidine dihydrochloride hydrate (FLIPR studies), phencyclidine hydrochloride (PCP), (+)MK-801 hydrogen maleate ([5R,10S]-[+]-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine), S(+)ketamine HCl and (-)nicotine hydrogen tartrate salt (Sigma-Aldrich, Saint Louis, Mo); methyllycaconitine citrate, (±)epibatidine (binding studies) and MDL-72222 (tropanyl 3,5-dichlorobenzoate BioTechne, Minneapolis, MN); [³H]granisetron ([³H]BRL-43694, specific activity 83.66 Ci/mmol, concentration 1 mCi/ml; Perkin Elmer, Waltham, MA).

Bristow L.J., Easton A.E., Li Y.W., Sivarao D.V., Lidge R., Jones K.M., Post-Munson D., Daly C., Lodge N.J., Gallagher L., Molski T., Pieschl R., Chen P., Hendricson A., Westphal R., Cook J., Iwuagwu C., Morgan D., Benitex Y., King D., Macor J.E., Zaczek R, & Olson R. (2016). The Novel, Nicotinic Alpha7 Receptor Partial Agonist, BMS-933043, Improves Cognition and Sensory Processing in Preclinical Models of Schizophrenia. PLoS ONE, 11(7), e0159996.

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