Evidence map›Paper›PMID 31935368›Full record

ArticleExperimental neurology2020

Ultrastructural and functional changes at the tripartite synapse during epileptogenesis in a model of temporal lobe epilepsy.

Cheryl Clarkson, Roy M Smeal, Meredith G Hasenoehrl, John A White, Maria E Rubio, Karen S Wilcox

Abstract read
In one paragraph

Article in Experimental neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Astrocytes and Epilepsy.Neurochemical research · 2021
    Article
  14. Article
  15. Review
  16. Neuromodulation of Glial Function During Neurodegeneration.Frontiers in cellular neuroscience · 2020
    Article
  17. Review
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Cheryl ClarksonDept. of Neurobiology, Univ. of Pittsburgh School of Medicine, Pittsburgh, PA 15261, United States of America.
Roy M SmealDept. of Pharmacology & Toxicology, University of Utah, Salt Lake City, UT 84112, United States of America.
Meredith G HasenoehrlInterdepartmental Program in Neuroscience, University of Utah, Salt Lake City, UT 84112, United States of America.
John A WhiteDept. of Biomedical Engineering, Boston University, Boston, MA 02215, United States of America.
Maria E RubioDept. of Neurobiology, Univ. of Pittsburgh School of Medicine, Pittsburgh, PA 15261, United States of America; Dept. of Otolaryngology, Univ. of Pittsburgh, Pittsburgh, PA 15261, United States of America. Electronic address: MER@pitt.edu.
Karen S WilcoxDept. of Pharmacology & Toxicology, University of Utah, Salt Lake City, UT 84112, United States of America; Interdepartmental Program in Neuroscience, University of Utah, Salt Lake City, UT 84112, United States of America. Electronic address: Karen.wilcox@hsc.utah.edu.

Funding

Calcium Signaling in a Model of Temporal Lobe EpilepsyR01NS078331 · NINDS · UNIVERSITY OF UTAH · PI WHITE, JOHN A., WILCOX, KAREN S · 2012 to 2016
$2.0M
Predoctoral Interdepartmental Training Program in NeuroscienceT32NS076067 · NINDS · UNIVERSITY OF UTAH · PI KEEFE, KRISTEN A · 2011 to 2015
$1.1M
NINDS NIH HHS R01 NS078331NINDS NIH HHS T32 NS076067
6 · The paper itself

Abstract

The persistent unresponsiveness of many of the acquired epilepsies to traditional antiseizure medications has motivated the search for prophylactic drug therapies that could reduce the incidence of epilepsy in this at risk population. These studies are based on the idea of a period of epileptogenesis that can follow a wide variety of brain injuries. Epileptogenesis is hypothesized to involve changes in the brain not initially associated with seizures, but which result finally in seizure prone networks. Understanding these changes will provide crucial clues for the development of prophylactic drugs. Using the repeated low-dose kainate rat model of epilepsy, we have studied the period of epileptogenesis following status epilepticus, verifying the latent period with continuous EEG monitoring. Focusing on ultrastructural properties of the tripartite synapse in the CA1 region of hippocampus we found increased astrocyte ensheathment around both the presynaptic and postsynaptic elements, reduced synaptic AMPA receptor subunit and perisynaptic astrocyte GLT-1 expression, and increased number of docked vesicles at the presynaptic terminal. These findings were associated with an increase in frequency of the mEPSCs observed in patch clamp recordings of CA1 pyramidal cells. The results suggest a complex set of changes, some of which have been associated with increasingly excitable networks such as increased vesicles and mEPSC frequency, and some associated with compensatory mechanisms, such as increased astrocyte ensheathment. The diversity of ultrastructural and electrophysiological changes observed during epileptogeneiss suggests that potential drug targets for this period should be broadened to include all components of the tripartite synapse.

Indexed as

AnimalsAstrocytesCA1 Region, HippocampalElectroencephalographyEpilepsy, Temporal LobeExcitatory Amino Acid AgonistsExcitatory Postsynaptic PotentialsKainic AcidMaleRatsRats, Sprague-DawleyReceptors, AMPAStatus EpilepticusSynapsesExcitatory Amino Acid AgonistsKainic AcidReceptors, AMPAAstrocyte ensheathmentElectron microscopyEpilepsyLatent periodmEPSCsPatch clampTripartite synapseUltrastructure

Identifiers

PMID31935368
PMCPMC7054984

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.