ArticleAdvances in pharmacological sciences2011
Augmentation of Tonic GABA(A) Inhibition in Absence Epilepsy: Therapeutic Value of Inverse Agonists at Extrasynaptic GABA(A) Receptors.
Article in Advances in pharmacological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Developmental Inhibitory Changes in the Primary Somatosensory Cortex of the Stargazer Mouse Model of Absence Epilepsy.Biomolecules · 2023Article
- Mechanisms of GABAergic and cholinergic neurotransmission in auditory thalamus: Impact of aging.Hearing research · 2021Review
- From Physiology to Pathology of Cortico-Thalamo-Cortical Oscillations: Astroglia as a Target for Further Research.Frontiers in neurology · 2021Review
- Sex Differences in the Epilepsies and Associated Comorbidities: Implications for Use and Development of Pharmacotherapies.Pharmacological reviews · 2020Review
- Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures.Brain : a journal of neurology · 2020Review
- Realising the therapeutic potential of neuroactive steroid modulators of the GABANeurobiology of stress · 2020Article
- Stimulus-induced Epileptic Spike-Wave Discharges in Thalamocortical Model with Disinhibition.Scientific reports · 2016Article
- Disinhibition-induced transitions between absence and tonic-clonic epileptic seizures.Scientific reports · 2015Article
- Novel astrocyte targets: new avenues for the therapeutic treatment of epilepsy.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2015Review
- A critical evaluation of the gamma-hydroxybutyrate (GHB) model of absence seizures.CNS neuroscience & therapeutics · 2015Review
- Activation of extrasynaptic GABA(A) receptors inhibits cyclothiazide-induced epileptiform activity in hippocampal CA1 neurons.Neuroscience bulletin · 2014Article
- ONO-2506 inhibits spike-wave discharges in a genetic animal model without affecting traditional convulsive tests via gliotransmission regulation.British journal of pharmacology · 2013Article
- New vistas on astroglia in convulsive and non-convulsive epilepsy highlight novel astrocytic targets for treatment.The Journal of physiology · 2013Review
- Extrasynaptic GABA(A) receptors: their function in the CNS and implications for disease.Neuron · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well established that impaired GABAergic inhibition within neuronal networks can lead to hypersynchronous firing patterns that are the typical cellular hallmark of convulsive epileptic seizures. However, recent findings have highlighted that a pathological enhancement of GABAergic signalling within thalamocortical circuits is a necessary and sufficient condition for nonconvulsive typical absence seizure genesis. In particular, increased activation of extrasynaptic GABA(A) receptors (eGABA(A)R) and augmented "tonic" GABA(A) inhibition in thalamocortical neurons have been demonstrated across a range of genetic and pharmacological models of absence epilepsy. Moreover, evidence from monogenic mouse models (stargazer/lethargic) and the polygenic Genetic Absence Epilepsy Rats from Strasbourg (GAERS) indicate that the mechanism underlying eGABA(A)R gain of function is nonneuronal in nature and results from a deficiency in astrocytic GABA uptake through the GAT-1 transporter. These results challenge the existing theory that typical absence seizures are underpinned by a widespread loss of GABAergic function in thalamocortical circuits and illustrate a vital role for astrocytes in the pathology of typical absence epilepsy. Moreover, they explain why pharmacological agents that enhance GABA receptor function can initiate or exacerbate absence seizures and suggest a potential therapeutic role for inverse agonists at eGABA(A)Rs in absence epilepsy.
Identifiers
What OpenQuestion holds
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.