Evidence map›Paper›PMID 31941661›Full record

ArticleeNeuro

TrkB Signaling Influences Gene Expression in Cortistatin-Expressing Interneurons.

Kristen R Maynard, Alisha Kardian, Julia L Hill, Yishan Mai, Brianna Barry, Henry L Hallock, Andrew E Jaffe, Keri Martinowich

Open access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. The basolateral amygdala to lateral septum circuit is critical for regulating social novelty in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  8. Genetic knockout ofFrontiers in cellular neuroscience · 2023
    Article
  9. Article
  10. Review
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

8 authors at 1 institution in 1 country.

Kristen R MaynardLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, Maryland 21205.ORCID 0000-0003-0031-8468
Alisha KardianLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, Maryland 21205.
Julia L HillLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, Maryland 21205.
Yishan MaiLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, Maryland 21205.
Brianna BarryLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, Maryland 21205.
Henry L HallockLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, Maryland 21205.
Andrew E JaffeLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, Maryland 21205.
Keri MartinowichLieber Institute for Brain Development, Johns Hopkins Medical Campus, Baltimore, Maryland 21205 Keri.martinowich@libd.org.ORCID 0000-0002-5237-0789
Johns Hopkins University · US

Funding

BIOCHEMISTRY, CELLULAR AND MOLECULAR BIOLOGY PROGRAMT32GM007445 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GREEN, RACHEL · 1985 to 2021
$24.1M
Regulation of neural activity in fear circuits by promoter IV derived BDNFR01MH105592 · NIMH · LIEBER INSTITUTE, INC. · PI MARTINOWICH, KERI · 2015 to 2024
$5.6M
NIGMS NIH HHS T32 GM007445NIMH NIH HHS R01 MH105592
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) signals through its cognate receptor tropomyosin receptor kinase B (TrkB) to promote the function of several classes of inhibitory interneurons. We previously reported that loss of BDNF-TrkB signaling in cortistatin (Cort)-expressing interneurons leads to behavioral hyperactivity and spontaneous seizures in mice. We performed bulk RNA sequencing (RNA-seq) from the cortex of mice with disruption of BDNF-TrkB signaling in cortistatin interneurons, and identified differential expression of genes important for excitatory neuron function. Using translating ribosome affinity purification and RNA-seq, we define a molecular profile for Cort-expressing inhibitory neurons and subsequently compare the translatome of normal and TrkB-depleted Cort neurons, revealing alterations in calcium signaling and axon development. Several of the genes enriched in Cort neurons and differentially expressed in TrkB-depleted neurons are also implicated in autism and epilepsy. Our findings highlight TrkB-dependent molecular pathways as critical for the maturation of inhibitory interneurons and support the hypothesis that loss of BDNF signaling in Cort interneurons leads to altered excitatory/inhibitory balance.

Indexed as

InterneuronsNeuropeptidesAnimalsBrain-Derived Neurotrophic FactorGene ExpressionMembrane GlycoproteinsMiceMice, Inbred C57BLProtein-Tyrosine KinasesReceptor, trkBBdnf protein, mouseBrain-Derived Neurotrophic FactorcortistatinMembrane GlycoproteinsNeuropeptidesNtrk2 protein, mouseProtein-Tyrosine KinasesReceptor, trkBASDBDNF-TrkBcortistatinepilepsyinhibitory interneuronsRibotag

Identifiers

PMID31941661
PMCPMC7031852
OpenAlexW3000431095

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.