Evidence map›Paper›PMID 24429870›Full record

ArticlePsychopharmacology2014

Pharmacological characterisation of ligand- and voltage-gated ion channels expressed in human iPSC-derived forebrain neurons.

Jeffrey L Dage, Ellen M Colvin, Antoine Fouillet, Emily Langron, William C Roell, Jingling Li, Sachin X Mathur, Adrian J Mogg, Matthew G Schmitt, Christian C Felder and 5 more

Abstract read
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In one paragraph

Article in Psychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 52 citations in OpenAlex.

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  8. An Epilepsy-Associated KCNT1 Mutation Enhances Excitability of Human iPSC-Derived Neurons by Increasing Slack KThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
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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

15 authors at 2 institutions in 2 countries.

Jeffrey L DageLilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN, 46285, USA.
Ellen M Colvin
Antoine Fouillet
Emily Langron
William C Roell
Jingling Li
Sachin X Mathur
Adrian J Mogg
Matthew G Schmitt
Christian C Felder
Kalpana M Merchant
John Isaac
Lisa M Broad
Emanuele Sher
Daniel Ursu
Eli Lilly (United States) · USEli Lilly (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGenetic causes, or predisposition, are increasingly accepted to be part of the ethiopathogenesis of many neuropsychiatric diseases. While genes can be studied in any type of cells, their physiological function in human brain cells is difficult to evaluate, particularly in living subjects.

methodsAs a first step towards the characterisation of human inducible pluripotent stem cell (iPSC)-derived neurons from autism spectrum disorder (ASD) patients, we used gene expression and functional studies to define the regional identity of the typical forebrain differentiation, demonstrate expression patterns of genes of interest in ASD and understand the properties of 'control' iPSC-derived neurons (iCell-Neurons™), with a focus on receptors and ion channels that play a central role in synaptic physio-pathology. RESULTS AND DISCUSSION: The gene expression profile of the iCell-Neurons™ closely resembled that observed in neonatal prefrontal cortex tissues. Functional studies, performed mainly using calcium flux assays, demonstrated the presence of ionotropic glutamate (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and N-methyl-D-aspartate) and gamma-aminobutyric acid type A receptors. Voltage-gated sodium and calcium channels were also identified using similar techniques.

conclusionsOverall, the results reported here suggest that iCell-Neurons™ are a good cellular model of a relatively immature forebrain human neuron population that can be used both as a control in comparison to patients cells, and as host cells in which mutations, insertions and deletions can be used in order to study the molecular mechanisms of ASD and other neurological disorders in an isogenic cellular background.

Indexed as

CalciumCalcium ChannelsGene ExpressionHumansInduced Pluripotent Stem CellsIon ChannelsMembrane PotentialsNeuronsProsencephalonReceptors, GABAReceptors, GABA-AReceptors, Ionotropic GlutamateReceptors, N-Methyl-D-AspartateRNA, MessengerTime FactorsVoltage-Gated Sodium ChannelsCalciumCalcium ChannelsIon ChannelsReceptors, GABAReceptors, GABA-AReceptors, Ionotropic GlutamateReceptors, N-Methyl-D-AspartateRNA, MessengerVoltage-Gated Sodium Channels

Identifiers

PMID24429870
OpenAlexW2039545195

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.