Evidence map›Paper›PMID 32401131›Full record

ArticleJournal of neurophysiology2020

BRAFV600E expression in neural progenitors results in a hyperexcitable phenotype in neocortical pyramidal neurons.

Roman U Goz, Gülcan Akgül, Joseph J LoTurco

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Ras-MAPK somatic variants in mesial temporal lobe epilepsy.Current opinion in genetics & development · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. The molecular landscape of glioblastoma-associated epilepsy.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. The mTOR pathway genesbioRxiv : the preprint server for biology · 2024
    Article
  12. Article
  13. Article
  14. OncogenicNeural regeneration research · 2023
    Article
  15. Article
  16. Review
  17. GABAScientific reports · 2022
    Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Roman U GozDepartment of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut.ORCID 0000-0002-7629-6544
Gülcan AkgülDepartment of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut.ORCID 0000-0003-1590-6350
Joseph J LoTurcoDepartment of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut.
University of Connecticut · US

Funding

Developmental Pathophysiology in Neocortex Caused By Somatic MutationsR01NS104999 · NINDS · UNIVERSITY OF CONNECTICUT STORRS · PI LOTURCO, JOSEPH J · 2018 to 2022
$1.8M
HHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS) R01NS104999NINDS NIH HHS R01 NS104999
6 · The paper itself

Abstract

Somatic mutations have emerged as the likely cause of focal epilepsies associated with developmental malformations and epilepsy-associated glioneuronal tumors (GNT). Somatic BRAFV600E mutations in particular have been detected in the majority of low-grade neuroepithelial tumors (LNETS) and in neurons in focal cortical dysplasias adjacent to epilepsy-associated tumors. Furthermore, conditional expression of an activating BRAF mutation in neocortex causes seizures in mice. In this study we characterized the cellular electrophysiology of layer 2/3 neocortical pyramidal neurons induced to express BRAFV600E from neural progenitor stages. In utero electroporation of a piggyBac transposase plasmid system was used to introduce transgenes expressing BRAF wild type (BRAFwt), BRAFV600E, and/or enhanced green fluorescent protein (eGFP) and monomeric red fluorescent protein (mRFP) into radial glia progenitors in mouse embryonic cortex. Whole cell patch-clamp recordings of pyramidal neurons in slices prepared from both juvenile and adult mice showed that BRAFV600E resulted in neurons with a distinct hyperexcitable phenotype characterized by depolarized resting membrane potentials, increased input resistances, lowered action potential (AP) thresholds, and increased AP firing frequencies. Some of the BRAFV600E-expressing neurons normally destined for upper cortical layers by their birthdate were stalled in their migration and occupied lower cortical layers. BRAFV600E-expressing neurons also displayed increased hyperpolarization-induced inward currents (

Indexed as

AnimalsCortical ExcitabilityElectrophysiological PhenomenaElectroporationEmbryo, MammalianFemaleMaleMiceNeocortexNeural Stem CellsPatch-Clamp TechniquesPhenotypePregnancyProto-Oncogene Proteins B-rafPyramidal CellsBraf protein, mouseProto-Oncogene Proteins B-rafBRAFV600Ecortical dysplasiaepilepsygangliogliomahyperexcitability

Identifiers

PMID32401131
PMCPMC7311733
OpenAlexW3025124464

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.