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
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 (
Original language | English |
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Journal | Journal of Neuroimmunology |
Volume | 251 |
Issue number | 1-2 |
Pages (from-to) | 65-72 |
Number of pages | 8 |
DOIs | |
Publication status | Published - 15 Oct 2012 |
- 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
Research areas
ID: 111179475