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Mecamylamine hydrochloride mec

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Mecamylamine hydrochloride (MEC) is a chemical compound used in research applications. It functions as a nicotinic acetylcholine receptor antagonist.

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Lab products found in correlation

Methyllycaconitine citrate mla, by Bio-Techne (6 mentions) Dihydro β erythroidine hydrobromide dhβe, by Bio-Techne (6 mentions) Bicuculline, by Merck Group (4 mentions) Carbenoxolone, by Bio-Techne (3 mentions) Tetrodotoxin ttx, by Merck Group (3 mentions) Scopolamine, by Bio-Techne (2 mentions) Vu0255035, by Bio-Techne (2 mentions) 4 aminopyridine 4 ap, by Bio-Techne (2 mentions) Cobalt chloride, by Merck Group (1 mentions) Choline bicarbonate, by Merck Group (1 mentions) Dopamine, by Merck Group (1 mentions) Nimodipine, by Merck Group (1 mentions) Amphetamine, by Merck Group (1 mentions) Sch 23390 hydrochloride, by Merck Group (1 mentions) Skf 38393 hydrochloride, by Merck Group (1 mentions) Flufenamic acid, by Merck Group (1 mentions) Bumetanide, by Merck Group (1 mentions) Picrotoxin, by Bio-Techne (1 mentions) Isoguvacine, by Merck Group (1 mentions) Gabazine, by Bio-Techne (1 mentions)

Spelling variants of this product

Mecamylamine (18 citations) Mecamylamine hydrochloride (8 citations)

6 protocols using mecamylamine hydrochloride mec

1

Pharmacological Blockade of Receptors

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Drugs that were used include bicuculline (10 μM, Sigma) to block GABAA receptors, Dihydro-b-erythroidine hydrobromide (DhβE; 1 μM, Tocris) to block type 2 nicotinic receptors, methyllycaconitine citrate (MLA; 500 nM, Tocris) as an antagonist of type I nicotinic receptors, mecamylamine hydrochloride (MEC; 5 μm, Tocris), CNQX (10 μM, Tocris) and APV (10 μM, Tocris) to block, respectively, AMPA and NMDA receptors.
Assous M., Kaminer J., Shah F., Garg A., Koós T, & Tepper J.M. (2017). Differential processing of thalamic information via distinct striatal interneuron circuits. Nature Communications, 8, 15860.
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2

Pharmacological Dissection of Striatal Neurotransmission

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We used bicuculline (10 μM, Sigma) to block GABAA receptors. Dihydro-β-erythroidine hydrobromide (DhβE; 1 μM, Tocris) was used to block nAChRs that contain β2-subunits including Type 2 nicotinic receptors (α4β2), and some heterormeric Type III nAChRs (β2*-containing). Methyllycaconitine citrate (MLA; 500 nM, Tocris) was used as an antagonist of nAChRs containing the α7 subunit (Type I nAChRs) mostly expressed presynaptically by glutamatergic afferents in the striatum, mecamylamine hydrochloride (MEC; 5 μm, Tocris) was used as a non-selective nAChRs antagonist that preferentially block Type III nAChRs [heterotrimeric α3β2β4, (Albuquerque et al., 1995 (link), 2009 (link))]. Atropine (Sigma, 10 μM) and scopolamine (Tocris, 10 μM) were used as non-selective mAChRs antagonists and VU0255035 (Tocris, 10 μM) as a selective M1 mAChR antagonist. CNQX (10 μM, Tocris) and APV (10 μM, Tocris) to block respectively AMPA and NMDA glutamate receptors. We used tetrodotoxin (TTX, 1 μM, Sigma) in association with 4-aminopyridine (4-AP, 200 μM, Tocris) to isolate monosynaptic responses. Finally, to block gap junction (electrotonic) communication we used carbenoxolone (100 μM, Tocris).
Kocaturk S., Guven E.B., Shah F., Tepper J.M, & Assous M. (2022). Cholinergic control of striatal GABAergic microcircuits. Cell reports, 41(4), 111531.
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3

Electrophysiological Recordings in Brain Slices

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Drugs were applied in the perfusion medium or locally via a micropipette using a Picospritzer (General Valve, Fairfield, NJ), at 20 psi / 30 – 100 ms, at 0.1 Hz. Cobalt chloride, nimodipine, flufenamic acid, SCH-23390 hydrochloride, SKF-38393 hydrochloride, dopamine, choline bicarbonate and amphetamine were purchased from Sigma-Aldrich and tetrodotoxin (TTX), carbamylcholine chloride (carbachol), mecamylamine hydrochloride (MEC), Dihydro-β-erythroidine hydrobromide (DHβE) and methyllycaconitine citrate (MLA) were purchased from Tocris. Cobalt chloride was prepared as an equimolar substitute for sucrose in modified Ringer’s solution. nimodipine and flufenamic acid were dissolved in dimethyl sulfoxide. All other drugs were dissolved freshly in Ringer’s solution.
Ibáñez-Sandoval O., Xenias H.S., Tepper J.M, & Koós T. (2015). Dopaminergic and Cholinergic Modulation of Striatal Tyrosine Hydroxylase Interneurons. Neuropharmacology, 95, 468-476.
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4

Pharmacological Dissection of Striatal Neurotransmission

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We used bicuculline (10 μM, Sigma) to block GABAA receptors. Dihydro-β-erythroidine hydrobromide (DhβE; 1 μM, Tocris) was used to block nAChRs that contain β2-subunits including Type 2 nicotinic receptors (α4β2), and some heterormeric Type III nAChRs (β2*-containing). Methyllycaconitine citrate (MLA; 500 nM, Tocris) was used as an antagonist of nAChRs containing the α7 subunit (Type I nAChRs) mostly expressed presynaptically by glutamatergic afferents in the striatum, mecamylamine hydrochloride (MEC; 5 μm, Tocris) was used as a non-selective nAChRs antagonist that preferentially block Type III nAChRs [heterotrimeric α3β2β4, (Albuquerque et al., 1995 (link), 2009 (link))]. Atropine (Sigma, 10 μM) and scopolamine (Tocris, 10 μM) were used as non-selective mAChRs antagonists and VU0255035 (Tocris, 10 μM) as a selective M1 mAChR antagonist. CNQX (10 μM, Tocris) and APV (10 μM, Tocris) to block respectively AMPA and NMDA glutamate receptors. We used tetrodotoxin (TTX, 1 μM, Sigma) in association with 4-aminopyridine (4-AP, 200 μM, Tocris) to isolate monosynaptic responses. Finally, to block gap junction (electrotonic) communication we used carbenoxolone (100 μM, Tocris).
Kocaturk S., Guven E.B., Shah F., Tepper J.M, & Assous M. (2022). Cholinergic control of striatal GABAergic microcircuits. Cell reports, 41(4), 111531.
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5

Pharmacological Modulation of Neuronal Activity

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SR 95531 hydrobromide (gabazine 5 μM, Tocris Bioscience, UK, Ref. 1262),2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione (NBQX, 10 µM, NIH generous gift), isoguvacine (10 μM, Sigma-Aldrich, Ref. G002), DL −2-Amino-5-phosphonovaleric acid (APV, 40 µM, Sigma-Aldrich, Ref. A5282), TTX (10 nM, 1 µM, Abcam, Bristol, UK, Ref. 120055), picrotoxin (50 µM, Tocris Bioscience, UK, Ref. 1128), ZD7288 (100 µM, Tocris Bioscience, UK, Ref. 1000), bumetanide (10 μM, Sigma-Aldrich, Ref. B3023) and the cocktail of nicotinic receptor antagonists including mecamylamine hydrochloride (MEC, 10 μM, Tocris Bioscience, Ref. 2843/10), methyllycaconitine citrate (MLA, 0.1 μM, Tocris Bioscience, Ref. 1029/5) and Dihydro-β-erythroidine hydrobromide (DHβE, 10 μM, Tocris Bioscience, Ref. 2349/10) were directly added to the perfusion solutions.
Lozovaya N., Eftekhari S, & Hammond C. (2023). The early excitatory action of striatal cholinergic-GABAergic microcircuits conditions the subsequent GABA inhibitory shift. Communications Biology, 6, 723.
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6

Pharmacological Modulation of Neural Circuits

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Drugs that were used include bicuculline (10μM, Sigma) to block GABA A receptors, Dihydro-βerythroidine hydrobromide (DhβE; 1μM, Tocris) to block type 2 nicotinic receptors (containing β2-subunits), methyllycaconitine citrate (MLA; 500nM, Tocris) as an antagonist of type I nicotinic receptors (containing α7-subunits), mecamylamine hydrochloride (MEC; 5 μm, Tocris), Atropine (Sigma, 10μM) to block muscarinic receptors, CNQX (10μM, Tocris) and APV (10μM, Tocris) to block respectively AMPA and NMDA glutamate receptors. To block gap junction (electrotonic) communication we used carbenoxolone (100μM, Tocris).
Kocatürk S., Shah F.A., GÜVEN B.B., Tepper J.M., & Assous M. (2021). Cholinergic control of striatal GABAergic microcircuits.
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