Evidence map›Paper›PMID 31711176›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2020

Cortical Foxp2 Supports Behavioral Flexibility and Developmental Dopamine D1 Receptor Expression.

Marissa Co, Stephanie L Hickey, Ashwinikumar Kulkarni, Matthew Harper, Genevieve Konopka

Open access · greenAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 38 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Marissa CoDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Stephanie L HickeyDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Ashwinikumar KulkarniDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Matthew HarperDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Genevieve KonopkaDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX, USA.
The University of Texas Southwestern Medical Center · US

Funding

The role of Foxp1-regulated signaling pathways in brain development and behaviorR01MH102603 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI KONOPKA, GENEVIEVE · 2015 to 2019
$2.2M
Functional dissection of mammalian vocal communicationR01DC014702 · NIDCD · UT SOUTHWESTERN MEDICAL CENTER · PI KONOPKA, GENEVIEVE · 2016 to 2020
$1.7M
Mechanisms of Disease & Translational ScienceT32GM109776 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI YIN, HELEN L · 2014 to 2018
$573k
UT Southwestern Center for Translational Medicine (UL18Kl2/TL1)TL1TR001104 · NCATS · UT SOUTHWESTERN MEDICAL CENTER · PI TOTO, ROBERT DANIEL · 2013 to 2017
$418k
Genes and Behavior: Reversible Knockdown of FoxP2 in Vocal LearningR21DC016340 · NIDCD · UT SOUTHWESTERN MEDICAL CENTER · PI KONOPKA, GENEVIEVE, ROBERTS, TODD F · 2017 to 2017
$324k
EPA EP-C-15-002NCATS NIH HHS TL1 TR001104NIDCD NIH HHS R01 DC014702NIDCD NIH HHS R21 DC016340NIGMS NIH HHS T32 GM109776NIMH NIH HHS R01 MH102603
6 · The paper itself

Abstract

Genetic studies have associated FOXP2 variation with speech and language disorders and other neurodevelopmental disorders (NDDs) involving pathology of the cortex. In this brain region, FoxP2 is expressed from development into adulthood, but little is known about its downstream molecular and behavioral functions. Here, we characterized cortex-specific Foxp2 conditional knockout mice and found a major deficit in reversal learning, a form of behavioral flexibility. In contrast, they showed normal activity levels, anxiety, and vocalizations, save for a slight decrease in neonatal call loudness. These behavioral phenotypes were accompanied by decreased cortical dopamine D1 receptor (D1R) expression at neonatal and adult stages, while general cortical development remained unaffected. Finally, using single-cell transcriptomics, we identified at least five excitatory and three inhibitory D1R-expressing cell types in neonatal frontal cortex, and we found changes in D1R cell type composition and gene expression upon cortical Foxp2 deletion. Strikingly, these alterations included non-cell-autonomous changes in upper layer neurons and interneurons. Together, these data support a role for Foxp2 in the development of dopamine-modulated cortical circuits and behaviors relevant to NDDs.

Indexed as

AnimalsBehavior, AnimalCerebral CortexCorpus StriatumForkhead Transcription FactorsGene Expression Regulation, DevelopmentalMiceMice, KnockoutNeuronsReceptors, Dopamine D1Repressor ProteinsReversal LearningDrd1 protein, mouseForkhead Transcription FactorsFoxp2 protein, mouseReceptors, Dopamine D1Repressor ProteinsdopamineFoxp2prefrontal cortexreversal learningsingle-cell RNA-seq

Identifiers

PMID31711176
PMCPMC7132914
OpenAlexW2985456447

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.