ArticlePloS one2013
γ-Hydroxybutyric acid (GHB) is not an agonist of extrasynaptic GABAA receptors.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 31 citations in OpenAlex.
- Interaction between γ-Hydroxybutyric Acid and Ethanol: A Review from Toxicokinetic and Toxicodynamic Perspectives.Metabolites · 2023Review
- Profiling of Primary Metabolites and Volatile Determinants in Mahlab Cherry (Foods (Basel, Switzerland) · 2021Article
- A multi-platform metabolomics approach identifies highly specific biomarkers of bacterial diversity in the vagina of pregnant and non-pregnant women.Scientific reports · 2015Article
- A critical evaluation of the gamma-hydroxybutyrate (GHB) model of absence seizures.CNS neuroscience & therapeutics · 2015Review
- Regulation of GABAARs by phosphorylation.Advances in pharmacology (San Diego, Calif.) · 2015Review
- GABAA receptor-acting neurosteroids: a role in the development and regulation of the stress response.Frontiers in neuroendocrinology · 2015Review
- GABA(B) receptor-mediated activation of astrocytes by gamma-hydroxybutyric acid.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Article
- Analysis of γ-aminobutyric acid (GABA) type A receptor subtypes using isosteric and allosteric ligands.Neurochemical research · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
γ-Hydroxybutyric acid (GHB) is an endogenous compound and a drug used clinically to treat the symptoms of narcolepsy. GHB is known to be an agonist of GABAB receptors with millimolar affinity, but also binds with much higher affinity to another site, known as the GHB receptor. While a body of evidence has shown that GHB does not bind to GABAA receptors widely, recent evidence has suggested that the GHB receptor is in fact on extrasynaptic α4β1δ GABAA receptors, where GHB acts as an agonist with an EC50 of 140 nM. We investigated three neuronal cell types that express a tonic GABAA receptor current mediated by extrasynaptic receptors: ventrobasal (VB) thalamic neurons, dentate gyrus granule cells and striatal medium spiny neurons. Using whole-cell voltage clamp in brain slices, we found no evidence that GHB (10 µM) induced any GABAA receptor mediated current in these cell types, nor that it modulated inhibitory synaptic currents. Furthermore, a high concentration of GHB (3 mM) was able to produce a GABAB receptor mediated current, but did not induce any other currents. These results suggest either that GHB is not a high affinity agonist at native α4β1δ receptors, or that these receptors do not exist in classical areas associated with extrasynaptic currents.
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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.