Evidence map›Paper›PMID 22279204›Full record

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

Increased excitatory synaptic input to granule cells from hilar and CA3 regions in a rat model of temporal lobe epilepsy.

Wei Zhang, John R Huguenard, Paul S Buckmaster

Open access · bronzeAbstract readComparative Study
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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Chemogenetics with PSAMGene therapy · 2025
    Article
  4. Article
  5. Microscale Neuronal Activity Collectively Drives Chaotic and Inflexible Dynamics at the Macroscale in Seizures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Deficits in Behavioral and Neuronal Pattern Separation in Temporal Lobe Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  10. Article
  11. Article
  12. Altered Synaptic Drive onto Birthdated Dentate Granule Cells in Experimental Temporal Lobe Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. TLR1 expression in mouse brain was increased in a KA-induced seizure model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015
    Article
  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

3 authors at 1 institution in 1 country.

Wei ZhangDepartment of Comparative Medicine, Stanford University, Stanford, California 94305-5342, USA.
John R Huguenard
Paul S Buckmaster
Stanford University · US

Funding

REGULATION OF NEURONAL EXCITABILITY IN CHRONIC EPILEPTOGENESISP50NS012151 · NINDS · STANFORD UNIVERSITY · PI BUCKMASTER, PAUL S. · 1985 to 2007
$9.1M
Ictogenesis in a model of temporal lobe epilepsyR01NS040276 · NINDS · STANFORD UNIVERSITY · PI BUCKMASTER, PAUL S. · 2000 to 2019
$5.8M
Inhibitory Controls of Thalamic NeuronsR01NS034774 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 1996 to 2021
$5.5M
Epilepsy Research ProgramP01NS012151 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 2008 to 2011
$4.4M
NINDS NIH HHS P01 NS012151NINDS NIH HHS P50 NS012151NINDS NIH HHS R01 NS034774NINDS NIH HHS R01 NS040276
6 · The paper itself

Abstract

One potential mechanism of temporal lobe epilepsy is recurrent excitation of dentate granule cells through aberrant sprouting of their axons (mossy fibers), which is found in many patients and animal models. However, correlations between the extent of mossy fiber sprouting and seizure frequency are weak. Additional potential sources of granule cell recurrent excitation that would not have been detected by markers of mossy fiber sprouting in previous studies include surviving mossy cells and proximal CA3 pyramidal cells. To test those possibilities in hippocampal slices from epileptic pilocarpine-treated rats, laser-scanning glutamate uncaging was used to randomly and focally activate neurons in the granule cell layer, hilus, and proximal CA3 pyramidal cell layer while measuring evoked EPSCs in normotopic granule cells. Consistent with mossy fiber sprouting, a higher proportion of glutamate-uncaging spots in the granule cell layer evoked EPSCs in epileptic rats compared with controls. In addition, stimulation spots in the hilus and proximal CA3 pyramidal cell layer were more likely to evoke EPSCs in epileptic rats, despite significant neuron loss in those regions. Furthermore, synaptic strength of recurrent excitatory inputs to granule cells from CA3 pyramidal cells and other granule cells was increased in epileptic rats. These findings reveal substantial levels of excessive, recurrent, excitatory synaptic input to granule cells from neurons in the hilus and proximal CA3 field. The aberrant development of these additional positive-feedback circuits might contribute to epileptogenesis in temporal lobe epilepsy.

Indexed as

Disease Models, AnimalAnimalsCA3 Region, HippocampalCerebellumEpilepsy, Temporal LobeExcitatory Postsynaptic PotentialsMaleNerve NetOrgan Culture TechniquesRatsRats, Sprague-Dawley

Identifiers

PMID22279204
PMCPMC3778651
OpenAlexW2072956069

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.