Evidence map›Paper›PMID 25229716›Full record

ArticleNeuropharmacology2015

Expression of GABA receptor subunits in the hippocampus and thalamus after experimental traumatic brain injury.

Meinrad Drexel, Noora Puhakka, Elke Kirchmair, Heide Hörtnagl, Asla Pitkänen, Günther Sperk

Open access · hybridAbstract read
In one paragraph

Article in Neuropharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Zolpidem Profoundly Augments Spared Tonic GABAFrontiers in systems neuroscience · 2022
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Tonic GABAergic inhibition, via GABAThe European journal of neuroscience · 2021
    Article
  18. Article
  19. The Emerging Roles of π Subunit-Containing GABAInternational journal of medical sciences · 2021
    Review
  20. Immunohistochemical distribution of 10 GABAThe Journal of comparative neurology · 2020
    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

6 authors at 3 institutions in 2 countries.

Meinrad DrexelDepartment of Pharmacology, Innsbruck Medical University, 6020 Innsbruck, Austria. Electronic address: Meinrad.drexel@i-med.ac.at.
Noora PuhakkaDepartment of Neurobiology, A. I. Virtanen Institute for Molecular Science, University of Eastern Finland, PO Box 1627, FI-70211 Kuopio, Finland.
Elke KirchmairDepartment of Pharmacology, Innsbruck Medical University, 6020 Innsbruck, Austria.
Heide HörtnaglDepartment of Pharmacology, Innsbruck Medical University, 6020 Innsbruck, Austria.
Asla PitkänenDepartment of Neurobiology, A. I. Virtanen Institute for Molecular Science, University of Eastern Finland, PO Box 1627, FI-70211 Kuopio, Finland; Department of Neurology, Kuopio University Hospital, PO Box 1777, FI-70211 Kuopio, Finland.
Günther SperkDepartment of Pharmacology, Innsbruck Medical University, 6020 Innsbruck, Austria.
Innsbruck Medical University · ATKuopio University Hospital · FIUniversity of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury is a major cause of death and disability worldwide and often associated with post-traumatic epilepsy. We recently demonstrated that TBI induces acquired GABAA receptors channelopathy that associates with hyperexcitability in granule cell layer (GCL). We now assessed the expression of GABAA and GABAB receptor subunit mRNAs between 6 h and 6 months post-TBI in the hippocampus and thalamus. The expression of major GABAA receptor subunit mRNAs (α1, α2, α5, β2, β3, γ2 and δ) was, often bilaterally, down-regulated in the GCL and in the CA3 pyramidal cells. Instead, expression of α4 (GCL, CA3, CA1), α5 (CA1) and γ2 (GCL, CA3, CA1) mRNA was up-regulated after 10 d and/or 4 months. Many of these changes were reversible. In the thalamus, we found decreases in α1, α4, β2, γ2 and δ mRNAs in the laterodorsal thalamus and in the area combining the posterior thalamic nuclear group, ventroposterolateral and ventroposteromedial complex at 6 h to 4 months post-TBI. Unlike in the hippocampus, thalamic subunit down-regulations were irreversible and limited to the ipsilateral side. However, contralaterally there was up-regulation of the subunits δ and α4 6 h and 4 months after TBI, respectively. PCR array analysis suggested a mild long-lasting GABAA receptor channelopathy in the GCL and thalamus after TBI. Whereas TBI induces transient changes in the expression of GABAA receptor subunits in the hippocampus (presumably representing compensatory mechanisms), alterations of GABAA receptor subunit mRNAs in the thalamus are long-lasting and related to degeneration of receptor-containing neurons in thalamo-cortical relay nuclei.

Indexed as

AnimalsAutoradiographyBrain InjuriesDisease Models, AnimalFunctional LateralityGene ExpressionHippocampusImmunohistochemistryIn Situ HybridizationLaser Capture MicrodissectionMaleRats, Sprague-DawleyReceptors, GABA-ARNA, MessengerThalamusReceptors, GABA-ARNA, MessengerEpilepsyGABALateral fluid-percussion injuryNeurosteroid

Identifiers

PMID25229716
PMCPMC4239297
OpenAlexW2019124093

What OpenQuestion holds

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LicenceCC BY
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.