Evidence map›Paper›PMID 20691786›Full record

ArticleNeurobiology of disease2010

Increased coupling and altered glutamate transport currents in astrocytes following kainic-acid-induced status epilepticus.

D K Takahashi, J R Vargas, K S Wilcox

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

63 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Astrocyte-neuron circuits in epilepsy.Neurobiology of disease · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Myo-Inositol Limits Kainic Acid-Induced Epileptogenesis in Rats.International journal of molecular sciences · 2022
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

D K TakahashiInterdepartmental Program in Neuroscience, University of Utah, Salt Lake City, UT 84108, USA.
J R Vargas
K S Wilcox
University of Utah · US

Funding

The Medial Entorhinal Cortex and Temporal Lobe EpilepsyR01NS044210 · NINDS · UNIVERSITY OF UTAH · PI WILCOX, KAREN S · 2003 to 2007
$1.3M
Astrocytes and temporal lobe epilepsyR21NS062419 · NINDS · UNIVERSITY OF UTAH · PI WILCOX, KAREN S · 2008 to 2009
$362k
Astrocyte Function and Temporal Lobe EpilepsyF31NS066774 · NINDS · UNIVERSITY OF UTAH · PI VARGAS, JAY ROBERT · 2009 to 2010
$55k
NINDS NIH HHS F31 NS066774NINDS NIH HHS NS044210NINDS NIH HHS NS062419NINDS NIH HHS NS066774NINDS NIH HHS R01 NS044210NINDS NIH HHS R21 NS062419
6 · The paper itself

Abstract

Profound astrogliosis coincident with neuronal cell loss is universally described in human and animal models of temporal lobe epilepsy (TLE). In the kainic acid-induced status epilepticus (SE) model of TLE, astrocytes in the hippocampus become reactive soon after SE and before the onset of spontaneous seizures. To determine if astrocytes in the hippocampus exhibit changes in function soon after SE, we recorded from SR101-labeled astrocytes using the whole-cell patch technique in hippocampal brain slices prepared from control and kainic-acid-treated rats. Glutamate transporter-dependent currents were found to have significantly faster decay time kinetics and in addition, dye coupling between astrocytes was substantially increased. Consistent with an increase in dye coupling in reactive astrocytes, immunoblot experiments demonstrated a significant increase in both glial fibrillary acidic protein (GFAP) and connexin 43, a major gap junction protein expressed by astrocytes. In contrast to what has been observed in resected tissue from patients with refractory epilepsy, changes in potassium currents were not observed shortly after KA-induced SE. While many changes in neuronal function have been identified during the initial period of low seizure probability in this model of TLE, the present study contributes to the growing body of literature suggesting a role for astrocytes in the process of epileptogenesis.

Indexed as

AnimalsAstrocytesBlotting, WesternBrainConnexin 43ConvulsantsGlial Fibrillary Acidic ProteinGlutamic AcidImmunohistochemistryKainic AcidMaleMicroscopy, ConfocalPatch-Clamp TechniquesRatsRats, Sprague-DawleyStatus EpilepticusConnexin 43ConvulsantsGlial Fibrillary Acidic ProteinGlutamic AcidKainic Acid

Identifiers

PMID20691786
PMCPMC3031166
OpenAlexW2160464539

What OpenQuestion holds

Textmetadata
LicenceTDM
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.