Evidence map›Paper›PMID 24672426›Full record

ReviewFrontiers in molecular neuroscience2014

Mechanisms regulating neuronal excitability and seizure development following mTOR pathway hyperactivation.

Candi L Lasarge, Steve C Danzer

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 194 citations in OpenAlex.

  1. Drug resistant epilepsy driven byEpilepsy & behavior reports · 2026
    Article
  2. Review
  3. Article
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  5. Review
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  7. Pathophysiology of Status Epilepticus Revisited.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Altered cortical excitability in tuberous sclerosis and the effect of mTOR inhibitors: An intracranial electrical stimulation study.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Focal postnatal deletion ofFrontiers in molecular neuroscience · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. Article

44 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

2 authors at 1 institution in 1 country.

Candi L LasargeDepartment of Anesthesia, Cincinnati Children's Hospital Medical Center Cincinnati, OH, USA.
Steve C DanzerDepartment of Anesthesia, Cincinnati Children's Hospital Medical Center Cincinnati, OH, USA ; Department of Anesthesia, University of Cincinnati Cincinnati, OH, USA ; Department of Pediatrics, University of Cincinnati Cincinnati, OH, USA.
Cincinnati Children's Hospital Medical Center · US

Funding

Selective disruption of hippocampal dentate granule cells in autism: impact of PTR01NS065020 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI DANZER, STEVE C · 2009 to 2023
$6.1M
mTOR regulation of aberrant neuronal integration and epileptogenesis in epilepsyR01NS062806 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI DANZER, STEVE C · 2009 to 2019
$3.6M
Contribution of abnormal granule cells to the development of an epileptic hippocaF32NS083239 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI LASARGE, CANDI LYNN · 2013 to 2013
$49k
NINDS NIH HHS F32 NS083239NINDS NIH HHS R01 NS062806NINDS NIH HHS R01 NS065020
6 · The paper itself

Abstract

The phosphatidylinositol-3-kinase/phosphatase and tensin homolog (PTEN)-mammalian target of rapamycin (mTOR) pathway regulates a variety of neuronal functions, including cell proliferation, survival, growth, and plasticity. Dysregulation of the pathway is implicated in the development of both genetic and acquired epilepsies. Indeed, several causal mutations have been identified in patients with epilepsy, the most prominent of these being mutations in PTEN and tuberous sclerosis complexes 1 and 2 (TSC1, TSC2). These genes act as negative regulators of mTOR signaling, and mutations lead to hyperactivation of the pathway. Animal models deleting PTEN, TSC1, and TSC2 consistently produce epilepsy phenotypes, demonstrating that increased mTOR signaling can provoke neuronal hyperexcitability. Given the broad range of changes induced by altered mTOR signaling, however, the mechanisms underlying seizure development in these animals remain uncertain. In transgenic mice, cell populations with hyperactive mTOR have many structural abnormalities that support recurrent circuit formation, including somatic and dendritic hypertrophy, aberrant basal dendrites, and enlargement of axon tracts. At the functional level, mTOR hyperactivation is commonly, but not always, associated with enhanced synaptic transmission and plasticity. Moreover, these populations of abnormal neurons can affect the larger network, inducing secondary changes that may explain paradoxical findings reported between cell and network functioning in different models or at different developmental time points. Here, we review the animal literature examining the link between mTOR hyperactivation and epileptogenesis, emphasizing the impact of enhanced mTOR signaling on neuronal form and function.

Indexed as

autismepilepsygranule cellshippocampusmTORneurogenesisPTENTSC

Identifiers

PMID24672426
PMCPMC3953715
OpenAlexW2070555834

What OpenQuestion holds

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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.