ArticlePloS one2011
Aberrant GABA(A) receptor-mediated inhibition in cortico-thalamic networks of succinic semialdehyde dehydrogenase deficient mice.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 36 citations in OpenAlex.
- Persistent input- and cell-type-specific synaptic alterations in the somatosensory thalamus of Dravet syndrome mice.Journal of neurophysiology · 2026Article
- Thalamic distribution and effects of 5-HT2C receptors on tonic GABAA inhibition and absence seizures: implications for treatment.Frontiers in pharmacology · 2026Article
- Suppressing astrocytic GABA transaminase enhances tonic inhibition and weakens hippocampal spatial memory.Experimental & molecular medicine · 2025Article
- Spike-and-wave discharges of absence seizures in a sleep waves-constrained corticothalamic model.CNS neuroscience & therapeutics · 2024Article
- ALDH5A1-deficient iPSC-derived excitatory and inhibitory neurons display cell type specific alterations.Neurobiology of disease · 2024Article
- GABA tone regulation and its cognitive functions in the brain.Nature reviews. Neuroscience · 2023Review
- From Physiology to Pathology of Cortico-Thalamo-Cortical Oscillations: Astroglia as a Target for Further Research.Frontiers in neurology · 2021Review
- The Critical Modulatory Role of Spiny Stellate Cells in Seizure Onset Based on Dynamic Analysis of a Neural Mass Model.Frontiers in neuroscience · 2021Article
- Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures.Brain : a journal of neurology · 2020Review
- Developmental changes of GABA immunoreactivity in cortico-thalamic networks of an absence seizure model.Neuropharmacology · 2018Article
- mTOR inhibitors rescue premature lethality and attenuate dysregulation of GABAergic/glutamatergic transcription in murine succinate semialdehyde dehydrogenase deficiency (SSADHD), a disorder of GABA metabolism.Journal of inherited metabolic disease · 2016Article
- Novel astrocyte targets: new avenues for the therapeutic treatment of epilepsy.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2015Review
- Altered intrathalamic GABAA neurotransmission in a mouse model of a human genetic absence epilepsy syndrome.Neurobiology of disease · 2015Article
- Central serotonin-2A (5-HT2A) receptor dysfunction in depression and epilepsy: the missing link?Frontiers in pharmacology · 2015Review
- Animal models of absence epilepsies: what do they model and do sex and sex hormones matter?Neurobiology of disease · 2014Review
- New vistas on astroglia in convulsive and non-convulsive epilepsy highlight novel astrocytic targets for treatment.The Journal of physiology · 2013Review
- Article
- From sleep spindles of natural sleep to spike and wave discharges of typical absence seizures: is the hypothesis still valid?Pflugers Archiv : European journal of physiology · 2012Review
- Augmentation of Tonic GABA(A) Inhibition in Absence Epilepsy: Therapeutic Value of Inverse Agonists at Extrasynaptic GABA(A) Receptors.Advances in pharmacological sciences · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Aberrant γ-aminobutyric acid type A (GABA(A)) receptor-mediated inhibition in cortico-thalamic networks remains an attractive mechanism for typical absence seizure genesis. Using the whole-cell patch clamp technique we examined 'phasic' and 'tonic' GABA(A) inhibition in thalamocortical neurons of somatosensory (ventrobasal, VB) thalamus, nucleus reticularis thalami (NRT) neurons, and layer 5/6 pyramidal neurons of the somatosensory (barrel) cortex of succinic semialdehyde dehydrogenase (SSADH) knock-out (SSADH(-/-)) mice that replicate human SSADH deficiency and exhibit typical absence seizures. We found increased sIPSC frequency in both VB and NRT neurons and larger sIPSC amplitude in VB neurons of SSADH(-/-) mice compared to wild-type animals, demonstrating an increase in total phasic inhibition in thalamus of SSADH(-/-) mice. mIPSCs in both VB and NRT neurons were no different between genotypes, although there remained a trend toward more events in SSADH(-/-) mice. In cortical layer 5/6 pyramidal neurons, sIPSCs were fewer but larger in SSADH(-/-) mice, a feature retained by mIPSCs. Tonic currents were larger in both thalamocortical neurons and layer 5/6 pyramidal neurons from SSADH(-/-) mice compared to WTs. These data show that enhanced, rather than compromised, GABA(A) receptor-mediated inhibition occurs in cortico-thalamic networks of SSADH(-/-) mice. In agreement with previous studies, GABA(A) receptor-mediated inhibitory gain-of-function may be a common feature in models of typical absence seizures, and could be of pathological importance in patients with SSADH deficiency.
Indexed as
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.