Cotinine (5S-1-methyl-5-(3-pyridyl) pyrrolidine-2-ona) was obtained from Sigma-Aldrich (Saint Louis, MO, United States). α4β2nAChR inhibitor dihydro-beta-erythroidine (DHβE) and the α7nAChR inhibitor, methyllycaconitine (MLA) were obtained from Tocris bioscience (Bristol, United Kingdom).
Methyllycaconitine mla
Manufactured by Bio-Techne
Sourced in United Kingdom, United States
Methyllycaconitine (MLA) is a naturally occurring alkaloid compound. It functions as a selective antagonist for the alpha7 nicotinic acetylcholine receptor (α7 nAChR). MLA is commonly used in research applications to study the pharmacological effects and mechanisms of α7 nAChR.
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Lab products found in correlation
Cotinine, by Merck Group (1 mentions)
Ly294002, by Selleck Chemicals (1 mentions)
Nicotine, by Merck Group (1 mentions)
Ab8049, by Abcam (1 mentions)
Ab12193, by Abcam (1 mentions)
Ecl plus reagent, by Merck Group (1 mentions)
Sirt1 assay kit, by Merck Group (1 mentions)
Trizol reagent, by Thermo Fisher Scientific (1 mentions)
Sybr green pcr master mix, by Thermo Fisher Scientific (1 mentions)
Nicotine ditartrate, by Bio-Techne (1 mentions)
Epibatidine, by Bio-Techne (1 mentions)
125i α bungarotoxin 125i α btx, by PerkinElmer (1 mentions)
3h epibatidine, by PerkinElmer (1 mentions)
Nicotine hydrogen tartrate salt, by Glentham Life Sciences (1 mentions)
Qx314 chloride qx314, by Merck Group (1 mentions)
D 2 amino 5 phosphonopentanoic acid d ap5, by Bio-Techne (1 mentions)
6 protocols using methyllycaconitine mla
1
Nicotinic Receptor Inhibitors Protocol
2
Nicotine-Induced Signaling Pathways
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Nicotine was purchased from Sigma-Aldrich (St. Louis, MO, USA), the α7-nAChR antagonist methyllycaconitine (MLA) was purchased from Tocris Bioscience (Bristol, England, UK), the P-AKT inhibitor Ly294002 was purchased from Selleck chemicals (Houston, TX, USA). All other chemicals were obtained from Sigma.
3
Alzheimer's Disease Biomarker Assessment
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RSV, Suramin, U0126 and the SIRT1 Assay Kit (Sigma-Aldrich, USA); methyllycaconitine (MLA) (Tocris Bioscience, UK); TRIzol reagent (Invitrogen, China), SYBR Green PCR master mix (Applied Biosystems, USA); ECL Plus reagent (Merck Millipore, Germany); the near-infrared amyloid-β fluorescent CRANAD-58 probe (ab146926, Abcam Inc., USA); rabbit monoclonal anti-p-Erk1/2 and rabbit monoclonal anti-Erk1/2 antibodies (4370 and 4695, Cell Signaling Technology (CST) Inc., USA); rabbit monoclonal anti-SIRT1 antibody and anti-SYP (synaptophysin) (ab12193 and ab8049; Abcam Inc., USA); rabbit polyclonal anti-α7 nAChR and mouse monoclonal anti-β-actin antibodies (sc-58607 and sc-376421, Santa Cruz Inc., USA); rabbit polyclonal anti SNAP-25 (synaptosomal-associated protein 25), rabbit polyclonal anti CREB, rabbit polyclonal anti CREB (phosphpo-Ser133), rabbit polyclonal anti GFAP and rabbit polyclonal anti-Iba-1 (ionized calcium binding adaptor molecule 1) antibodies (GTX113839, GTX112846, GTX130379, GTX108711 and GTX100042, Gentex Inc., USA) and horseradish peroxidase-conjugated secondary antibody (7076s and 7074s, CST Inc., USA) were obtained from the sources indicated.
4
Nicotine and BDNF Receptor Study
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The (-)-nicotine ditartrate (Tocris Bioscience, Bristol, United Kingdom), brain-derived neurotrophic factor (BDNF) (Alomone Labs Ltd., Jerusalem, Israel) and nAChR antagonists α-conotoxin MII (α-CTX MII), α-conotoxin PIA (α-CTX PIA), mecamylamine (MEC), dihydro-β-erythroidine (DHβE), and methyllycaconitine (MLA) (Tocris Bioscience) were used in the present study and are detailed in Supplementary Table S1 . For each vehicle treatment, solvents required by specific drugs were used at the same dilution used for the active treatment.
5
Binding Assays for Nicotinic Receptors
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20-methyl spirolide G (≥97% purity), obtained from laboratory cultures of the dinoflagellate Alexandrium ostenfeldii, was purchased from Cifga (Lugo, Spain). [125I]α−Bungarotoxin ([125I]α−BTX) (210–250 Ci·mmol−1), and (±)[3H]epibatidine (55 Ci·mmol−1), were purchased from PerkinElmer (Courtaboeuf, France). Isoflurane (AErrane®) was purchased from Baxter S.A. (Lessines, Belgium). Other chemicals were obtained from Sigma-Aldrich (Saint Quentin Fallavier, France), or other standard sources. The α-toxin from Naja nigricollis was synthesized, refolded, and purified, as previously described [30 (link)]. Methyllycaconitine (MLA), and (±)epibatidine were purchased from Tocris Bioscience (Bristol, UK).
6
Pharmacological Modulation of Neuronal Receptors
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