Evidence map›Paper›PMID 20631216›Full record

ArticleJournal of neurophysiology2010

Excitatory input onto hilar somatostatin interneurons is increased in a chronic model of epilepsy.

Brian Halabisky, Isabel Parada, Paul S Buckmaster, David A Prince

Abstract readComparative Study
In one paragraph

Article in Journal of neurophysiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

44 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
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  4. Interneuron theta phase locking controls seizure susceptibility.bioRxiv : the preprint server for biology · 2025
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  10. Heterozygous expression of abioRxiv : the preprint server for biology · 2024
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  15. Article
  16. Adult Born Dentate Granule Cell Mediated Upregulation of Feedback Inhibition in a Mouse Model of Traumatic Brain Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  17. Article
  18. Adaptive Mossy Cell Circuit Plasticity after Status Epilepticus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  19. Zolpidem Profoundly Augments Spared Tonic GABAFrontiers in systems neuroscience · 2022
    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

4 authors at 1 institution in 1 country.

Brian HalabiskyStanford University School of Medicine, Department of Neurology, Stanford, CA 94305, USA.
Isabel Parada
Paul S Buckmaster
David A Prince
Stanford University · US

Funding

MODULATION OF NEOCORTICAL INTERNEURONAL FUNCTIONR01NS039579 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R, PRINCE, DAVID ALLAN · 2000 to 2013
$4.3M
NINDS NIH HHS R01 NS039579
6 · The paper itself

Abstract

The density of somatostatin (SOM)-containing GABAergic interneurons in the hilus of the dentate gyrus is significantly decreased in both human and experimental temporal lobe epilepsy. We used the pilocarpine model of status epilepticus and temporal lobe epilepsy in mice to study anatomical and electrophysiological properties of surviving somatostatin interneurons and determine whether compensatory functional changes occur that might offset loss of other inhibitory neurons. Using standard patch-clamp techniques and pipettes containing biocytin, whole cell recordings were obtained in hippocampal slices maintained in vitro. Hilar SOM cells containing enhanced green fluorescent protein (EGFP) were identified with fluorescent and infrared differential interference contrast video microscopy in epileptic and control GIN (EGFP-expressing Inhibitory Neurons) mice. Results showed that SOM cells from epileptic mice had 1) significant increases in somatic area and dendritic length; 2) changes in membrane properties, including a small but significant decrease in resting membrane potential, and increases in time constant and whole cell capacitance; 3) increased frequency of slowly rising spontaneous excitatory postsynaptic currents (sEPSCs) due primarily to increased mEPSC frequency, without changes in the probability of release; 4) increased evoked EPSC amplitude; and 5) increased spontaneous action potential generation in cell-attached recordings. Results suggest an increase in excitatory innervation, perhaps on distal dendrites, considering the slower rising EPSCs and increased output of hilar SOM cells in this model of epilepsy. In sum, these changes would be expected to increase the inhibitory output of surviving SOM interneurons and in part compensate for interneuronal loss in the epileptogenic hippocampus.

Indexed as

Disease Models, AnimalAnimalsChronic DiseaseDentate GyrusEpilepsyExcitatory Postsynaptic PotentialsFemaleInterneuronsMaleMiceOrgan Culture TechniquesSomatostatinSomatostatin

Identifiers

PMID20631216
PMCPMC3774571
OpenAlexW2051753774

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.