Evidence map›Paper›PMID 22496577›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Adenosine release during seizures attenuates GABAA receptor-mediated depolarization.

Andrei Ilie, Joseph V Raimondo, Colin J Akerman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 78 citations in OpenAlex.

  1. GABACellular and molecular neurobiology · 2026
    Review
  2. Review
  3. Article
  4. Optogenetic Determination of Dynamic and Cell-Type-Specific Inhibitory Reversal Potentials.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Disrupting Epileptiform Activity by Preventing Parvalbumin Interneuron Depolarization Block.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  10. Review
  11. Unique Actions of GABA Arising from Cytoplasmic Chloride Microdomains.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
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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.

Andrei IlieDepartment of Pharmacology, Oxford University, Oxford OX1 3QT, United Kingdom.
Joseph V Raimondo
Colin J Akerman
University of Oxford · GB

Funding

Biotechnology and Biological Sciences Research Council BB/E015476/1Biotechnology and Biological Sciences Research Council BB/E0154761European Research Council 243273Medical Research Council G0601503Wellcome Trust
6 · The paper itself

Abstract

Seizure-induced release of the neuromodulator adenosine is a potent endogenous anticonvulsant mechanism, which limits the extension of seizures and mediates seizure arrest. For this reason several adenosine-based therapies for epilepsy are currently under development. However, it is not known how adenosine modulates GABAergic transmission in the context of seizure activity. This may be particularly relevant as strong activation of GABAergic inputs during epileptiform activity can switch GABA(A) receptor (GABA(A)R) signaling from inhibitory to excitatory, which is a process that plays a significant role in intractable epilepsies. We used gramicidin-perforated patch-clamp recordings to investigate the role of seizure-induced adenosine release in the modulation of postsynaptic GABA(A)R signaling in pyramidal neurons of rat hippocampus. Consistent with previous reports, GABA(A)R responses during seizure activity transiently switched from hyperpolarizing to depolarizing and excitatory. We found that adenosine released during the seizure significantly attenuated the depolarizing GABA(A)R responses and also reduced the extent of the after-discharge phase of the seizure. These effects were mimicked by exogenous adenosine administration and could not be explained by a change in chloride homeostasis mechanisms that set the reversal potential for GABA(A)Rs, or by a change in the conductance of GABA(A)Rs. Rather, A(1)R-dependent activation of potassium channels increased the cell's membrane conductance and thus had a shunting effect on GABA(A)R currents. As depolarizing GABA(A)R signaling has been implicated in seizure initiation and progression, the adenosine-induced attenuation of depolarizing GABA(A)R signaling may represent an important mechanism by which adenosine can limit seizure activity.

Indexed as

AdenosineAdenosine A1 Receptor AgonistsAnimalsCA3 Region, HippocampalChloridesEpilepsy, Temporal LobeGABA AgonistsGramicidinIn Vitro TechniquesMaleMembrane PotentialsMuscimolNeural ConductionPatch-Clamp TechniquesPyramidal CellsRatsAdenosineAdenosine A1 Receptor AgonistsChloridesGABA AgonistsGramicidinMuscimolReceptors, GABA-ATetrodotoxin

Identifiers

PMID22496577
PMCPMC6622092
OpenAlexW2050845257

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.