The α7 nicotinic acetylcholine receptor ligands methyllycaconitine, NS6740 and GTS-21 reduce lipopolysaccharide-induced TNF-α release from microglia

Research output: Contribution to journal › Journal article › Research

Standard

The α7 nicotinic acetylcholine receptor ligands methyllycaconitine, NS6740 and GTS-21 reduce lipopolysaccharide-induced TNF-α release from microglia. / Thomsen, Morten Skøtt; Mikkelsen, Jens D.

In: Journal of Neuroimmunology, Vol. 251, No. 1-2, 15.10.2012, p. 65-72.

Research output: Contribution to journal › Journal article › Research

Harvard

Thomsen, MS & Mikkelsen, JD 2012, 'The α7 nicotinic acetylcholine receptor ligands methyllycaconitine, NS6740 and GTS-21 reduce lipopolysaccharide-induced TNF-α release from microglia', Journal of Neuroimmunology, vol. 251, no. 1-2, pp. 65-72. https://doi.org/10.1016/j.jneuroim.2012.07.006

APA

Thomsen, M. S., & Mikkelsen, J. D. (2012). The α7 nicotinic acetylcholine receptor ligands methyllycaconitine, NS6740 and GTS-21 reduce lipopolysaccharide-induced TNF-α release from microglia. Journal of Neuroimmunology, 251(1-2), 65-72. https://doi.org/10.1016/j.jneuroim.2012.07.006

Vancouver

Thomsen MS, Mikkelsen JD. The α7 nicotinic acetylcholine receptor ligands methyllycaconitine, NS6740 and GTS-21 reduce lipopolysaccharide-induced TNF-α release from microglia. Journal of Neuroimmunology. 2012 Oct 15;251(1-2):65-72. https://doi.org/10.1016/j.jneuroim.2012.07.006

Author

Thomsen, Morten Skøtt ; Mikkelsen, Jens D. / The α7 nicotinic acetylcholine receptor ligands methyllycaconitine, NS6740 and GTS-21 reduce lipopolysaccharide-induced TNF-α release from microglia. In: Journal of Neuroimmunology. 2012 ; Vol. 251, No. 1-2. pp. 65-72.

Bibtex

@article{fc58709508624756925652f0e0e6a740,
title = "The α7 nicotinic acetylcholine receptor ligands methyllycaconitine, NS6740 and GTS-21 reduce lipopolysaccharide-induced TNF-α release from microglia",
abstract = "The anti-inflammatory properties of, particularly the α7, nicotinic acetylcholine receptors (nAChRs) in the peripheral immune system are well documented. There are also reports of anti-inflammatory actions of nicotine in the CNS, but it is unclear, whether this is due to activation or inhibition of nAChRs. Here we investigate the mechanisms behind α7 nAChR-mediated modulation of TNF-α release. We show that α7 nAChR agonists or positive allosteric modulators do not affect LPS-induced release of the pro-inflammatory cytokine TNF-α from cultured microglia. This suggests that classical activation of, i.e. ion-flux through, the α7 nAChR does not reduce TNF-α release from activated microglia. Contrarily, the α7 nAChR antagonist methyllycaconitine and the weak (",
keywords = "Aconitine, Animals, Anti-Inflammatory Agents, Azabicyclo Compounds, Benzylidene Compounds, Furans, Lipopolysaccharides, MAP Kinase Signaling System, Male, Microglia, Nicotinic Agonists, Nicotinic Antagonists, Pyridines, Rats, Rats, Sprague-Dawley, Receptors, Nicotinic, Tumor Necrosis Factor-alpha, alpha7 Nicotinic Acetylcholine Receptor",
author = "Thomsen, {Morten Sk{\o}tt} and Mikkelsen, {Jens D}",
note = "Copyright {\textcopyright} 2012 Elsevier B.V. All rights reserved.",
year = "2012",
month = oct,
day = "15",
doi = "10.1016/j.jneuroim.2012.07.006",
language = "English",
volume = "251",
pages = "65--72",
journal = "Journal of Neuroimmunology",
issn = "0165-5728",
publisher = "Elsevier",
number = "1-2",

}

RIS

TY - JOUR

T1 - The α7 nicotinic acetylcholine receptor ligands methyllycaconitine, NS6740 and GTS-21 reduce lipopolysaccharide-induced TNF-α release from microglia

AU - Thomsen, Morten Skøtt

AU - Mikkelsen, Jens D

N1 - Copyright © 2012 Elsevier B.V. All rights reserved.

PY - 2012/10/15

Y1 - 2012/10/15

N2 - The anti-inflammatory properties of, particularly the α7, nicotinic acetylcholine receptors (nAChRs) in the peripheral immune system are well documented. There are also reports of anti-inflammatory actions of nicotine in the CNS, but it is unclear, whether this is due to activation or inhibition of nAChRs. Here we investigate the mechanisms behind α7 nAChR-mediated modulation of TNF-α release. We show that α7 nAChR agonists or positive allosteric modulators do not affect LPS-induced release of the pro-inflammatory cytokine TNF-α from cultured microglia. This suggests that classical activation of, i.e. ion-flux through, the α7 nAChR does not reduce TNF-α release from activated microglia. Contrarily, the α7 nAChR antagonist methyllycaconitine and the weak (

AB - The anti-inflammatory properties of, particularly the α7, nicotinic acetylcholine receptors (nAChRs) in the peripheral immune system are well documented. There are also reports of anti-inflammatory actions of nicotine in the CNS, but it is unclear, whether this is due to activation or inhibition of nAChRs. Here we investigate the mechanisms behind α7 nAChR-mediated modulation of TNF-α release. We show that α7 nAChR agonists or positive allosteric modulators do not affect LPS-induced release of the pro-inflammatory cytokine TNF-α from cultured microglia. This suggests that classical activation of, i.e. ion-flux through, the α7 nAChR does not reduce TNF-α release from activated microglia. Contrarily, the α7 nAChR antagonist methyllycaconitine and the weak (

KW - Aconitine

KW - Animals

KW - Anti-Inflammatory Agents

KW - Azabicyclo Compounds

KW - Benzylidene Compounds

KW - Furans

KW - Lipopolysaccharides

KW - MAP Kinase Signaling System

KW - Male

KW - Microglia

KW - Nicotinic Agonists

KW - Nicotinic Antagonists

KW - Pyridines

KW - Rats

KW - Rats, Sprague-Dawley

KW - Receptors, Nicotinic

KW - Tumor Necrosis Factor-alpha

KW - alpha7 Nicotinic Acetylcholine Receptor

U2 - 10.1016/j.jneuroim.2012.07.006

DO - 10.1016/j.jneuroim.2012.07.006

M3 - Journal article

C2 - 22884467

VL - 251

SP - 65

EP - 72

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

SN - 0165-5728

IS - 1-2

ER -

ID: 111179475