In vitro and in vivo effects of an α3 neuronal nicotinic acetylcholine receptor antisense oligonucleotide

2004 ◽  
Vol 129 (1-2) ◽  
pp. 67-79 ◽  
Author(s):  
Monique R. Adams ◽  
Arthur L. Nikkel ◽  
Diana L. Donnelly-Roberts ◽  
Andrew T. Watt ◽  
Joseph F. Johnston ◽  
...  
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Antisense Oligonucleotide ◽  
Neuronal Nicotinic Acetylcholine Receptor ◽  
Nicotinic Acetylcholine ◽  
In Vivo Effects

scholarly journals Synthesis, nicotinic acetylcholine receptor binding, in vitro and in vivo pharmacology properties of 3′-(substituted pyridinyl)-deschloroepibatidine analogs

2015 ◽  
Vol 23 (17) ◽  
pp. 5693-5701 ◽  
Author(s):  
Pauline W. Ondachi ◽  
Zhuo Ye ◽  
Ana H. Castro ◽  
Charles W. Luetje ◽  
M. Imad Damaj ◽  
...  
Keyword(s):  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Receptor Binding ◽  
Nicotinic Acetylcholine

scholarly journals Autophagy is Involved in Neuroprotective Effect of Alpha7 Nicotinic Acetylcholine Receptor on Ischemic Stroke

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhe-Qi Xu ◽  
Jing-Jing Zhang ◽  
Ni Kong ◽  
Guang-Yu Zhang ◽  
Ping Ke ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Acetylcholine Receptor ◽  
Nicotinic Acetylcholine Receptor ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Autophagy Flux ◽  
Nicotinic Acetylcholine

The α7 nicotinic acetylcholine receptor (α7nAChR) belongs to the superfamily of cys loop cationic ligand-gated channels, which consists of homogeneous α7 subunits. Although our lab found that activation of α7nAChR could alleviate ischemic stroke, the mechanism is still unknown. Herein, we explored whether autophagy is involved in the neuroprotective effect mediated by α7nAChR in ischemic stroke. Transient middle cerebral artery occlusion (tMCAO) and oxygen and glucose deprivation (OGD/R) exposure were applied to in vivo and in vitro models of ischemic stroke, respectively. Neurological deficit score and infarct volume were used to evaluate outcomes of tMCAO in the in vivo study. Autophagy-related proteins were detected by Western blot, and autophagy flux was detected by using tandem fluorescent mRFP-GFP-LC3 lentivirus. At 24 h after tMCAO, α7nAChR knockout mice showed worse neurological function and larger infarct volume than wild-type mice. PNU282987, an α7nAChR agonist, protected against OGD/R-induced neuronal injury, enhanced autophagy, and promoted autophagy flux. However, the beneficial effects of PNU282987 were eliminated by 3-methyladenine (3-MA), an autophagy inhibitor. Moreover, we found that PNU282987 treatment could activate the AMPK-mTOR-p70S6K signaling pathway in the in vitro study, while the effect was attenuated by compound C, an AMPK inhibitor. Our results demonstrated that the beneficial effect on neuronal survival via activation of α7nAChR was associated with enhanced autophagy, and the AMPK-mTOR-p70S6K signaling pathway was involved in α7nAChR activation–mediated neuroprotection.

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