Evidence map›Paper›PMID 30187194›Full record

ArticleBrain structure & function2018

Foxp2 loss of function increases striatal direct pathway inhibition via increased GABA release.

Jon-Ruben van Rhijn, Simon E Fisher, Sonja C Vernes, Nael Nadif Kasri

Abstract read
In one paragraph

Article in Brain structure & function, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The transcription factorFrontiers in cell and developmental biology · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. An Etiological Foxp2 Mutation Impairs Neuronal Gain in Layer VI Cortico-Thalamic Cells through Increased GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  11. FOXP transcription factors in vertebrate brain development, function, and disorders.Wiley interdisciplinary reviews. Developmental biology · 2020
    Review
  12. 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.

Jon-Ruben van RhijnDepartment of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboudumc, 6525 HR, Nijmegen, The Netherlands.
Simon E FisherLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, 6525 XD, Nijmegen, The Netherlands.
Sonja C VernesNeurogenetics of Vocal Communication Group, Max Planck Institute for Psycholinguistics, 6525 XD, Nijmegen, The Netherlands. Sonja.vernes@mpi.nl.
Nael Nadif KasriDepartment of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboudumc, 6525 HR, Nijmegen, The Netherlands. n.nadif@donders.ru.nl.ORCID http://orcid.org/0000-0002-7448-9289

Funding

FP7 People: Marie-Curie Actions PCIG12-GA-2012-333978
6 · The paper itself

Abstract

Heterozygous mutations of the Forkhead-box protein 2 (FOXP2) gene in humans cause childhood apraxia of speech. Loss of Foxp2 in mice is known to affect striatal development and impair motor skills. However, it is unknown if striatal excitatory/inhibitory balance is affected during development and if the imbalance persists into adulthood. We investigated the effect of reduced Foxp2 expression, via a loss-of-function mutation, on striatal medium spiny neurons (MSNs). Our data show that heterozygous loss of Foxp2 decreases excitatory (AMPA receptor-mediated) and increases inhibitory (GABA receptor-mediated) currents in D1 dopamine receptor positive MSNs of juvenile and adult mice. Furthermore, reduced Foxp2 expression increases GAD67 expression, leading to both increased presynaptic content and release of GABA. Finally, pharmacological blockade of inhibitory activity in vivo partially rescues motor skill learning deficits in heterozygous Foxp2 mice. Our results suggest a novel role for Foxp2 in the regulation of striatal direct pathway activity through managing inhibitory drive.

Indexed as

Excitatory Postsynaptic PotentialsInhibitory Postsynaptic PotentialsAnimalsCorpus StriatumForkhead Transcription Factorsgamma-Aminobutyric AcidGlutamate DecarboxylaseLearningMice, Inbred C57BLMice, TransgenicMotor SkillsNeuronsReceptors, Dopamine D1Repressor ProteinsSynapsesForkhead Transcription FactorsFoxp2 protein, mousegamma-Aminobutyric AcidGlutamate Decarboxylaseglutamate decarboxylase 1Receptors, Dopamine D1Repressor ProteinsD1R-MSNExcitatory-inhibitory balanceFoxp2NeurodevelopmentStriatum

Identifiers

PMID30187194
PMCPMC6267273

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.