ReviewCurrent neuropharmacology2019
Application of the Co-Agonist Concerted Transition Model to Analysis of GABAA Receptor Properties.
Review in Current neuropharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Effects of ivermectin on the activation and desensitization of the human GABAMolecular pharmacology · 2026Article
- Activation of the human β3 GABABiochemical pharmacology · 2026Article
- Null method to estimate the maximal PA at subsaturating concentrations of agonist.The Journal of general physiology · 2025Article
- Direct measurements of neurosteroid binding to specific sites on GABABritish journal of pharmacology · 2024Article
- State-dependent energetics of GABABiophysical journal · 2024Article
- Potentiation of the GABABiophysical journal · 2024Article
- Mutational Analysis of Anesthetic Binding Sites and Their Effects on GABABiomolecules · 2023Article
- Modulation of the mammalian GABABritish journal of pharmacology · 2022Article
- Activation of the α1β2γ2L GABABiomolecules · 2021Article
- A critical residue in the αeLife · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The co-agonist concerted transition model is a simple and practical solution to analyze various aspects of GABAA receptor function. Several model-based predictions have been verified experimentally in previous reports. We review here the practical implications of the model and demonstrate how it enables simplification of the experimental procedure and data analysis to characterize the effects of mutations or properties of novel ligands. Specifically, we show that the value of EC50 and the magnitude of current response are directly affected by basal activity, and that coapplication of a background agonist acting at a distinct site or use of a gain-of-function mutation can be employed to enable studies of weak activators or mutated receptors with impaired gating. We also show that the ability of one GABAergic agent to potentiate the activity elicited by another is a computable value that depends on the level of constitutive activity of the ion channel and the ability of each agonist to directly activate the receptor. Significantly, the model accurately accounts for situations where the paired agonists interact with the same site compared to distinct sites on the receptor.
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