ArticleThe Journal of general physiology2020
Mechanism of calcium potentiation of the α7 nicotinic acetylcholine receptor.
Article in The Journal of general physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- The relationship between apparent potentiation and the magnitude of the control response.The Journal of general physiology · 2026Article
- Article
- Key role of the TM2-TM3 loop in calcium potentiation of the α9α10 nicotinic acetylcholine receptor.Cellular and molecular life sciences : CMLS · 2024Article
- Novel interplay between agonist and calcium binding sites modulates drug potentiation of α7 acetylcholine receptor.Cellular and molecular life sciences : CMLS · 2024Article
- Structural bases for stoichiometry-selective calcium potentiation of a neuronal nicotinic receptor.British journal of pharmacology · 2024Article
- Channelopathies in epilepsy: an overview of clinical presentations, pathogenic mechanisms, and therapeutic insights.Journal of neurology · 2024Review
- Nicotine: From Discovery to Biological Effects.International journal of molecular sciences · 2023Review
- Generation of nanobodies acting as silent and positive allosteric modulators of the α7 nicotinic acetylcholine receptor.Cellular and molecular life sciences : CMLS · 2023Article
- Derepression may masquerade as activation in ligand-gated ion channels.Nature communications · 2023Article
- Stoichiometry-selective modulation of α4β2 nicotinic ACh receptors by divalent cations.British journal of pharmacology · 2022Article
- Chromosomal Microarray Analysis as First-Tier Genetic Test for Schizophrenia.Frontiers in genetics · 2021Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The α7 nicotinic acetylcholine receptor (nAChR) is among the most abundant types of nAChR in the brain, yet the ability of nerve-released ACh to activate α7 remains enigmatic. In particular, a major population of α7 resides in extra-synaptic regions where the ACh concentration is reduced, owing to dilution and enzymatic hydrolysis, yet ACh shows low potency in activating α7. Using high-resolution single-channel recording techniques, we show that extracellular calcium is a powerful potentiator of α7 activated by low concentrations of ACh. Potentiation manifests as robust increases in the frequency of channel opening and the average duration of the openings. Molecular dynamics simulations reveal that calcium binds to the periphery of the five ligand binding sites and is framed by a pair of anionic residues from the principal and complementary faces of each site. Mutation of residues identified by simulation prevents calcium from potentiating ACh-elicited channel opening. An anionic residue is conserved at each of the identified positions in all vertebrate species of α7. Thus, calcium associates with a novel structural motif on α7 and is an obligate cofactor in regions of limited ACh concentration.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.