Mecamylamine hydrochloride

Manufactured by Merck Group

Sourced in United States, Germany, United Kingdom

Mecamylamine hydrochloride is a chemical compound used as a laboratory reagent. It is a nicotinic acetylcholine receptor antagonist. The core function of this product is to serve as a research tool for studying nicotinic receptor-mediated processes in various in vitro and in vivo experimental models.

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Lab products found in correlation

51 protocols using mecamylamine hydrochloride

Cardiovascular Pharmacology Reagents

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ACR, ethylene glycol tetra-acetic acid (EGTA), atropine, mecamylamine hydrochloride, Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME), nereistoxin (NTX), and phenylephrine (PE) were purchased from Sigma-Aldrich (Saint Louis, MO, USA). Sodium chloride, KCl, calcium chloride dehydrate, potassium dihydrogen phosphate, magnesium sulphate heptahydrate, sodium hydrogen carbonate, and glucose were purchased from Merck (Darmstadt, Germany).

Lin W.D., Ou C.C., Hsiao S.H., Chang C.H., Tsai F.J., Liao J.W, & Chen Y.T. (2021). Effects of Acrylamide-Induced Vasorelaxation and Neuromuscular Blockage: A Rodent Study. Toxics, 9(6), 117.

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Nicotine and Mecamylamine Dosing Protocol

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(−)-Nicotine hydrogen tartrate salt [(−)-1-Methyl-2-(3-pyridyl) pyrrolidine (+)-bitartrate salt], (-)-menthol and mecamylamine hydrochloride were purchased from Sigma-Aldrich (St. Louis, MO). All drugs except for menthol were dissolved in physiological saline (0.9% sodium chloride) and injected at a total volume of 1ml/100 g body weight unless noted otherwise. Menthol was dissolved in a mixture of 1:1:18 [1 volume ethanol/1 volume Emulphor-620 (Rhone-Poulenc, Inc., Princeton, NJ) and 18 volumes distilled water] and administered intraperitoneal (i.p.). All doses are expressed as the free base of the drug. Mecamylamine and nicotine were injected subcutaneously (s.c.).

Alsharari S.D., King J.R., Nordman J.C., Muldoon P.P., Jackson A., Zhu A.Z., Tyndale R.F., Kabbani N, & Damaj M.I. (2015). Effects of Menthol on Nicotine Pharmacokinetic, Pharmacology and Dependence in Mice. PLoS ONE, 10(9), e0137070.

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Investigating the Modulatory Effects of CRP and Nicotinic Antagonists on Cytokine Release in LPS-Primed U937 Cells

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U937 cells (DSMZ, Braunschweig, Germany) were maintained in RPMI 1640 (Gibco by Life Technologies, Darmstadt, Germany) supplemented with 10% fetal calf serum (FCS, Biochrome, Berlin, Germany) and 2 mM l-glutamine (Gibco by Life Technologies) under 5% CO₂ atmosphere at 37°C. Cells (1 × 10⁶ cells/ml) were seeded in 24-well plates, primed for 5 h with 1 µg/ml lipopolysaccharide (LPS) from Escherichia coli (L2654, Sigma-Aldrich, Deisenhofen, Germany) (30 (link)). BzATP [2′(3′)-O-(4-benzoylbenzoyl)adenosine 5′-triphosphate triethylammonium salt; 100 µM, Sigma-Aldrich] or nigericin (50 µM, Sigma-Aldrich) were added for another 30 min in the presence or absence of different concentrations of eCRP from human pleural fluid (Millipore, AG732), recombinant CRP (rCRP) produced in E. coli (Millipore, 236608), serum amyloid P (SAP; Millipore, 565190), or PC chloride calcium salt tetrahydrate (Sigma-Aldrich). Nicotinic antagonists mecamylamine hydrochloride (Sigma-Aldrich), strychnine hydrochloride (Sigma-Aldrich), α-bungarotoxin (Tocris Bioscience, Bristol, UK), ArIB [V11L, V16D] (500 nM) (34 (link), 35 (link)) and RgIA4 (200 nM) (31 (link), 36 (link)) were also applied together with BzATP. Supernatants were stored at 20°C until cytokine and lactate dehydrogenase (LDH) measurement.

Richter K., Sagawe S., Hecker A., Küllmar M., Askevold I., Damm J., Heldmann S., Pöhlmann M., Ruhrmann S., Sander M., Schlüter K.D., Wilker S., König I.R., Kummer W., Padberg W., Hone A.J., McIntosh J.M., Zakrzewicz A.T., Koch C, & Grau V. (2018). C-Reactive Protein Stimulates Nicotinic Acetylcholine Receptors to Control ATP-Mediated Monocytic Inflammasome Activation. Frontiers in Immunology, 9, 1604.

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Nicotine Exposure and Withdrawal

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Vapour exposures used either mint nicotine JUUL pods (30:70 PG:VG; 59 mg/ml nicotine; JUUL Labs, Washington D.C., United States) or mint vehicle JUUL pods (30:70 PG:VG, 10% mint flavour; E-Cigz vape shop, Guelph, ON). Mecamylamine hydrochloride (1.5 mg/kg in saline; Sigma-Aldrich) was used for withdrawal experiments.

Frie J.A., McCunn P., Eed A., Hassan A., Luciani K.R., Chen C., Tyndale R.F, & Khokhar J.Y. (2023). Factors influencing JUUL e-cigarette nicotine vapour-induced reward, withdrawal, pharmacokinetics and brain connectivity in rats: sex matters. Neuropsychopharmacology, 49(5), 782-795.

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Acute Cholinergic Modulation of Forced Swim Test

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Adult male mice (n = 178; n=16-18 per group) were acclimated to daily intraperitoneal (i.p) injections of saline one week prior to drug testing to minimize acute stress on test day. Thirty minutes prior to FST, mice received either i.p. saline or 0.03 mg/kg of the AChE inhibitor physostigmine to decrease ACh breakdown. Animals then received a second i.p. injection of the nAChR antagonist mecamylamine (Rabenstein, et al, 2006 (link) Sigma, mecamylamine hydrochloride, 0.56 or 0.75 mg/kg, 30 minutes pre-FST), the mAChR antagonist scopolamine (Witkin et al, 2014 (link), Sigma, scopolamine hydrobromide, 0.03 or 0.065 mg/kg, 10 min pre-FST), or saline (20 min pre-FST). Statistical effects were queried using ANOVA with photoperiod, and drug treatment as factors. Hypothesized a priori effects of physostigmine were queried using specific one-way ANOVA.

Cope Z.A., Lavadia M.L., Joosen A.J., van de Cappelle C.J., Lara J.C., Huval A., Kwiatkowski M.K., Picciotto M.R., Mineur Y.S., Dulcis D, & Young J.W. (2020). Converging evidence that short-active photoperiod increases acetylcholine signaling in the hippocampus. Cognitive, affective & behavioral neuroscience, 20(6), 1173-1183.

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Investigating α7nAChR Signaling in Rodent Models

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Sprague-Dawley rats (230∼270 g) and C57BL/6 mice (25∼30 g) were purchased from Sino-British SIPPR/BK Laboratory Animals (Shanghai, China). α7^-/- mice were generated and genotyped by PCR analysis as described previously (Liu et al., 2009 (link)). Animals were housed at 22°C under a 12/12 light schedule (on: 08:00), with free access to tap water and standard rat chow. All experimental procedures were in accordance with institutional animal care guidelines and approved by ethics committee of Second Military Medical University. Ani (Ani hydrochloride: C₁₇H₂₄NO₄) was purchased from Fu-Ma Chemical and Engineering Company (Hangzhou, China). Mecamylamine hydrochloride, methyllycaconitine (MLA) citrate, hexamethonium chloride, ACh chloride, nicotine, PNU282987 (PNU), static, ouabain octahydrate, potassium chloride, and antibody against α7nAChR were purchased from Sigma–Aldrich (St. Louis, MO, USA). HNMPA-(AM)3 and antibody against p-Na/K-ATPase were purchased from Santa Cruz Biotechnology (Dallas, TX, USA). antibody against insulin receptor, Alexa-488-labeled and Cy3-labeled second antibodies, and DAPI were purchased from Abcam (Cambridge, MA, USA). LY 294002 and rapamycin were purchased from Merck Millipore (Darmstadt, Germany).

Fan B.S., Zhang E.H., Wu M., Guo J.M., Su D.F., Liu X, & Yu J.G. (2016). Activation of α7 Nicotinic Acetylcholine Receptor Decreases On-site Mortality in Crush Syndrome through Insulin Signaling-Na/K-ATPase Pathway. Frontiers in Pharmacology, 7, 79.

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Nicotine and Mecamylamine Delivery Protocol

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Nicotine bitartrate and mecamylamine hydrochloride (Sigma Chemical Co., St. Louis, MO) were dissolved in sterile saline. The pH of the nicotine solution was adjusted to 7.4 with dilute NaOH. Nicotine doses are expressed as the base. Nicotine was administered via osmotic minipump (see below). Mecamylamine was administered via s.c. injection at a volume of 1.0 ml/kg.

Muelken P., Schmidt C.E., Shelley D., Tally L, & Harris A.C. (2015). A Two-Day Continuous Nicotine Infusion Is Sufficient to Demonstrate Nicotine Withdrawal in Rats as Measured Using Intracranial Self-Stimulation. PLoS ONE, 10(12), e0144553.

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Mecamylamine-Induced Nicotine Withdrawal in Zebrafish

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In the Group B to assess mecamylamine-induced withdrawal the non-selective nAChR antagonist mecamylamine hydrochloride (Sigma-Aldrich, MO, USA) was injected intramuscularly (i.m.) at a dose of (1 mg/kg i.m.) dissolved in its vehicle (sterile saline, 0.9%). The dose was chosen based on previous studies on nicotine withdrawal in mice (Ponzoni et al., 2015 (link)). On day 14, fish (20 for each group) were divided into four groups: exposure to nicotine +vehicle (saline), exposure to nicotine + mecamylamine (1 mg/kg, i.m.); drug-free exposure +vehicle; drug-free exposure+ mecamylamine. Precipitated nicotine withdrawal assessment was performed immediately after treatment.
Swimming activity and freezing behaviour (physical signs of nicotine withdrawal) were evaluated in a swimming tank divided into ten equal-sized 2 × 10 cm rectangles marked with permanent marker on the floor (Swain et al. 2004 (link)). The number of crossed lines was measured counting the number of lines crossed in a 30-s observation period, every min for a total of 5 observation bins, over 5 min, according to Ponzoni et al. (2014) (link). Freezing behaviour, sign of anxiety was defined as a total absence of movement, except for the gills and eyes for > 2 sec, as reported by Stewart et al. (2015) (link). At the end of the behavioural experiments zebrafish were killed.

Ponzoni L., Melzi G., Marabini L., Martini A., Petrillo G., Teh M.T., Torres-Perez J.V., Morara S., Gotti C., Braida D., Brennan C.H, & Sala M. (2021). Conservation of mechanisms regulating emotional-like responses on spontaneous nicotine withdrawal in zebrafish and mammals. Progress in neuro-psychopharmacology & biological psychiatry, 111, 110334.

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Targeted Neuromodulation for Operant Behavior

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All drugs were delivered 10 min before animals performed the PR test, through an opto-fluid system chronically implanted in the NAc. Injections were performed using a 5-μl gastight seringe (Hamilton), attached to the implanted injection cannula of the rats through 22-gauge tubing, at a constant rate of 1 μl/min.
The drugs used in experimental procedures were: R(+)-SCH-23390 hydrochloride (D1R antagonist, 0.25 μg in 0.5 μl of saline, Sigma); (S)-(-)-sulpiride (D2R antagonist, 0.2 μg in 1 μl, Sigma); scopolamine hydrobromide [muscarinic acetylcholine receptor (mAChR) antagonist, 25 μg in 1 μl, Sigma]; mecamylamine hydrochloride (nAChR antagonist, 22.5 μg in 1 μl, Sigma); Ddihydro-β-erythroidine hydrobromide (DHβE, α4-nAChR antagonist, 0.7 μg in 1 μl, Tocris); CGP-55845 hydrochloride (GABA(B) receptor antagonist, 44 ng in 0.5 μl, Sigma); 1(S),9(R)-(-)-bicuculine methobromide (GABA(A) receptor antagonist, 75 ng in 0.5 μl, Sigma).

Soares-Cunha C., Coimbra B., Domingues A.V., Vasconcelos N., Sousa N, & Rodrigues A.J. (2018). Nucleus Accumbens Microcircuit Underlying D2-MSN-Driven Increase in Motivation. eNeuro, 5(2), ENEURO.0386-18.2018.

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Nicotine, Heparin, and Meloxicam Protocol

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Nicotine hydrogen tartrate salt was obtained from Glentham Life Sciences (catalog #GL9693-5G). Injectable heparin sodium (catalog #07-892-8971) and injectable meloxicam (catalog #07-891-7959) were obtained from Patterson Veterinary Supply. Mecamylamine hydrochloride was obtained from Sigma-Aldrich (catalog #M9020).

Tapia M.A., Jin X.T., Tucker B.R., Thomas L.N., Walker N.B., Kim V.J., Albertson S.E., Damuka N., Krizan I., Edassery S., Savas J.N., Sai K.K., Jones S.R, & Drenan R.M. (2022). Relapse-like behavior and nAChR sensitization following intermittent access nicotine self-administration. Neuropharmacology, 212, 109066.

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