ArticleJournal of neuroscience research2013
γ-Aminobutyric acid type A receptor inhibition triggers a nicotinic neuroprotective mechanism.
Article in Journal of neuroscience research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Memantine has a nicotinic neuroprotective pathway in acute hippocampal slices after an NMDA insult.Toxicology in vitro : an international journal published in association with BIBRA · 2022Article
- In Vivo Evaluation of the Acute Systemic Toxicity of (1S,2E,4R,6R,7E,11E)-Cembratriene-4,6-diol (4R) in Sprague Dawley Rats.Nutraceuticals · 2022Article
- 4R-cembranoid confers neuroprotection against LPS-induced hippocampal inflammation in mice.Journal of neuroinflammation · 2021Article
- A Review on Bioactivities of Tobacco Cembranoid Diterpenes.Biomolecules · 2019Review
- 4R-Cembranoid Improves Outcomes after 6-Hydroxydopamine Challenge in BothFrontiers in neuroscience · 2017Article
- Pharmacokinetics and Metabolism of 4R-Cembranoid.PloS one · 2015Article
- 4R-cembranoid protects against diisopropylfluorophosphate-mediated neurodegeneration.Neurotoxicology · 2014Article
- Kinin-B2 receptor exerted neuroprotection after diisopropylfluorophosphate-induced neuronal damage.Neuroscience · 2013Article
- Protective activity of (1S,2E,4R,6R,7E,11E)-2,7,11-cembratriene-4,6-diol analogues against diisopropylfluorophosphate neurotoxicity: preliminary structure-activity relationship and pharmacophore modeling.Bioorganic & medicinal chemistry · 2013Article
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Authors and funding
6 authors.
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Abstract
Nicotinic acetylcholine receptor (nAChR)-mediated neuroprotection has been implicated in the treatment of neurodegenerative disorders such as Alzheimer's and Parkinson's diseases and hypoxic ischemic events as well as other diseases hallmarked by excitotoxic and apoptotic neuronal death. Several modalities of nicotinic neuroprotection have been reported. However, although this process generally involves α4β2 and α7 subtypes, the underlying mechanisms are largely unknown. Interestingly, both activation and inhibition of α7 nAChRs have been reported to be neuroprotective. We have shown that inhibition of α7 nAChRs protects the function of acute hippocampal slices against excitotoxicity in an α4β2-dependent manner. Neuroprotection was assessed as the prevention of the N-methyl-D-aspartate-dependent loss of the area of population spikes (PSs) in the CA1 area of acute hippocampal slices. Our results support a model in which α7 AChRs control the release of γ-aminobutyric acid (GABA). Blocking either α7 or GABA(A) receptors reduces the inhibitory tone on cholinergic terminals, thereby promoting α4β2 activation, which in turn mediates neuroprotection. These results shed light on how α7 nAChR inhibition can be neuroprotective through a mechanism mediated by activation of α4β2 nAChRs.
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