Evidence map›Paper›PMID 24262146›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Astrocytes potentiate GABAergic transmission in the thalamic reticular nucleus via endozepine signaling.

Catherine A Christian, John R Huguenard

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 57 citations in OpenAlex.

  1. Acyl-CoA-binding protein as a driver of pathological aging.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Article
  3. Voltage-gated potassium channels control extended access cocaine seeking: a role for nucleus accumbens astrocytes.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  4. Article
  5. Integrins Bidirectionally Regulate the Efficacy of Inhibitory Synaptic Transmission and Control GABAergic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  6. Review
  7. Astrocytes: GABAceptive and GABAergic Cells in the Brain.Frontiers in cellular neuroscience · 2022
    Review
  8. Review
  9. αACS chemical neuroscience · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Physiology of Astroglia.Physiological reviews · 2018
    Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Catherine A ChristianDepartment of Neurology and Neurological Sciences, Stanford University, Stanford, CA 94305.
John R Huguenard
Stanford University · US

Funding

Inhibitory Controls of Thalamic NeuronsR01NS034774 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 1996 to 2021
$5.5M
CELLULAR MECHANISMS IN FOCAL EPILEPTOGENESISR01NS006477 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 1985 to 2013
$5.0M
EPILEPSY TRAINING PROGRAMT32NS007280 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 1985 to 2020
$3.6M
NINDS NIH HHS R01 NS006477NINDS NIH HHS R01 NS034774NINDS NIH HHS T32 NS007280
6 · The paper itself

Abstract

Emerging evidence indicates that diazepam-binding inhibitor (DBI) mediates an endogenous benzodiazepine-mimicking (endozepine) effect on synaptic inhibition in the thalamic reticular nucleus (nRT). Here we demonstrate that DBI peptide colocalizes with both astrocytic and neuronal markers in mouse nRT, and investigate the role of astrocytic function in endozepine modulation in this nucleus by testing the effects of the gliotoxin fluorocitrate (FC) on synaptic inhibition and endozepine signaling in the nRT using patch-clamp recordings. FC treatment reduced the effective inhibitory charge of GABAA receptor (GABAAR)-mediated spontaneous inhibitory postsynaptic currents in WT mice, indicating that astrocytes enhance GABAAR responses in the nRT. This effect was abolished by both a point mutation that inhibits classical benzodiazepine binding to GABAARs containing the α3 subunit (predominant in the nRT) and a chromosomal deletion that removes the Dbi gene. Thus, astrocytes are required for positive allosteric modulation via the α3 subunit benzodiazepine-binding site by DBI peptide family endozepines. Outside-out sniffer patches pulled from neurons in the adjacent ventrobasal nucleus, which does not contain endozepines, show a potentiated response to laser photostimulation of caged GABA when placed in the nRT. FC treatment blocked the nRT-dependent potentiation of this response, as did the benzodiazepine site antagonist flumazenil. When sniffer patches were placed in the ventrobasal nucleus, however, subsequent treatment with FC led to potentiation of the uncaged GABA response, suggesting nucleus-specific roles for thalamic astrocytes in regulating inhibition. Taken together, these results suggest that astrocytes are required for endozepine actions in the nRT, and as such can be positive modulators of synaptic inhibition.

Indexed as

Allosteric RegulationAnimalsAstrocytesCitratesDiazepam Binding InhibitorGABAergic NeuronsGliotoxinIntralaminar Thalamic NucleiMicePatch-Clamp TechniquesReceptors, GABA-ASignal TransductionSynaptic TransmissionCitratesDiazepam Binding InhibitorGliotoxingliotoxin fluorocitrateReceptors, GABA-Aelectrophysiologyepilepsygliathalamusuncaging

Identifiers

PMID24262146
PMCPMC3864346
OpenAlexW2063199361

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.