ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
A portable site: a binding element for 17β-estradiol can be placed on any subunit of a nicotinic α4β2 receptor.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Systemically circulating 17β-estradiol enhances the neuroprotective effect of the smoking cessation drug cytisine in female parkinsonian mice.NPJ Parkinson's disease · 2025Article
- Sex and estradiol effects in the rodent dorsal striatum.The European journal of neuroscience · 2024Review
- Estradiol treatment in young postmenopausal women with self-reported cognitive complaints: Effects on cholinergic-mediated cognitive performance.Human psychopharmacology · 2022Article
- Sex differences in dopamine release regulation in the striatum.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Review
- Sex Differences in the Nicotinic Acetylcholine Receptor System of Rodents: Impacts on Nicotine and Alcohol Reward Behaviors.Frontiers in neuroscience · 2021Review
- Heterologous expression of concatenated nicotinic ACh receptors: Pros and cons of subunit concatenation and recommendations for construct designs.British journal of pharmacology · 2020Article
- Discovery of an intrasubunit nicotinic acetylcholine receptor-binding site for the positive allosteric modulator Br-PBTC.The Journal of biological chemistry · 2019Article
- The molecular nature of the 17β-Estradiol binding site in the voltage- and CaScientific reports · 2019Article
- Orthosteric and allosteric potentiation of heteromeric neuronal nicotinic acetylcholine receptors.British journal of pharmacology · 2018Review
- Nicotinic acetylcholine receptors at the single-channel level.British journal of pharmacology · 2018Review
- Concatenated nicotinic acetylcholine receptors: A gift or a curse?The Journal of general physiology · 2018Article
- Determination of the Residues in the Extracellular Domain of the NicotinicMolecular pharmacology · 2017Article
- Unraveling amino acid residues critical for allosteric potentiation of (α4)3(β2)2-type nicotinic acetylcholine receptor responses.The Journal of biological chemistry · 2017Article
- α2* Nicotinic acetylcholine receptors influence hippocampus-dependent learning and memory in adolescent mice.Learning & memory (Cold Spring Harbor, N.Y.) · 2017Article
- The E Loop of the Transmitter Binding Site Is a Key Determinant of the Modulatory Effects of Physostigmine on Neuronal Nicotinic α4β2 Receptors.Molecular pharmacology · 2017Article
- Role of the Cys Loop and Transmembrane Domain in the Allosteric Modulation of α4β2 Nicotinic Acetylcholine Receptors.The Journal of biological chemistry · 2017Article
- A Novel α2/α4 Subtype-selective Positive Allosteric Modulator of Nicotinic Acetylcholine Receptors Acting from the C-tail of an α Subunit.The Journal of biological chemistry · 2015Article
- Article
- The nicotinic α5 subunit can replace either an acetylcholine-binding or nonbinding subunit in the α4β2* neuronal nicotinic receptor.Molecular pharmacology · 2014Article
- A neurosteroid potentiation site can be moved among GABAA receptor subunits.The Journal of physiology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Endogenous steroids can modulate the activity of transmitter-gated channels by directly interacting with the receptor. 17β-Estradiol potentiates activation of neuronal nicotinic α4β2 receptors by interacting with a 4 aa sequence at the extreme C terminus of the α4 subunit, but it is not known whether potentiation requires that the sequence be placed on a specific subunit (e.g., an α4 subunit that is involved in forming an acetylcholine-binding site). By using concatemers of subunits and chimeric subunits, we have found that the C-terminal domain can be moved from the α4 to the β2 subunit and still result in potentiation. In addition, the sequence can be placed on a subunit that contributes to an acetylcholine-binding site or on the structural subunit. The data indicate that this estradiol-binding element is a discrete sequence and suggest that the effect of 17β-estradiol is mediated by actions on single subunits and that the overall consequences for gating occur because of the summation of independent energetic contributions to overall gating of this receptor.
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Registered trials
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.