Evidence map›Paper›PMID 23548689›Full record

ArticleDevelopmental neuroscience2013

Prenatal expression of MET receptor tyrosine kinase in the fetal mouse dorsal raphe nuclei and the visceral motor/sensory brainstem.

Hsiao-Huei Wu, Pat Levitt

Open access · bronzeAbstract read
In one paragraph

Article in Developmental neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Development and regeneration of the vagus nerve.Seminars in cell & developmental biology · 2024
    Review
  3. Article
  4. Article
  5. Dorsal raphe organization.Journal of chemical neuroanatomy · 2020
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Serotonin neuron abnormalities in the BTBR mouse model of autism.Autism research : official journal of the International Society for Autism Research · 2017
    Article
  14. Article
  15. Review
  16. Hepatocyte Growth Factor-c-MET Signaling Mediates the Development of Nonsensory Structures of the Mammalian Cochlea and Hearing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  17. Article
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Hsiao-Huei WuDepartment of Cell and Neurobiology, Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California, Los Angeles, Calif. 90089, USA.
Pat Levitt
University of California, San Diego · US

Funding

Function &Structure Adaptation in Forebrain DevelopmentR01MH067842 · NIMH · VANDERBILT UNIVERSITY · PI LEVITT, PAT · 2002 to 2023
$10.8M
Stress-Mediated Alterations in Serotonin 2C Receptor Editing and FunctionP50MH096972 · NIMH · VANDERBILT UNIVERSITY · PI BLAKELY, RANDY D. · 2012 to 2016
$10.5M
Function and Structure Adaptations in Forebrain DevelopmentR56MH067842 · NIMH · CHILDREN'S HOSPITAL OF LOS ANGELES · PI LEVITT, PAT · 2014 to 2014
$662k
Mechanisms of Autonomic Brainstem DevelopmentR21NS086413 · NINDS · CHILDREN'S HOSPITAL OF LOS ANGELES · PI LEVITT, PAT · 2014 to 2015
$446k
NIMH NIH HHS MH067842NIMH NIH HHS P50 MH096972NIMH NIH HHS R01 MH067842NIMH NIH HHS R56 MH067842NINDS NIH HHS R21 NS086413
6 · The paper itself

Abstract

Signaling via MET receptor tyrosine kinase (MET) has been implicated in a number of neurodevelopmental events, including cell migration, dendritic and axonal development and synaptogenesis. Related to its role in the development of forebrain circuitry, we recently identified a functional promoter variant of the MET gene that is associated with autism spectrum disorder (ASD). The association of the MET promoter variant rs1858830 C allele is significantly enriched in families with a child who has ASD and co-occurring gastrointestinal conditions. The expression of MET in the forebrain had been mapped in detail in the developing mouse and rhesus macaque. However, in mammals, its expression in the developing brainstem has not been studied extensively throughout developmental stages. Brainstem and autonomic circuitry are implicated in ASD pathophysiology and in gastrointestinal dysfunction. To advance our understanding of the neurodevelopmental influences of MET signaling in brainstem circuitry development, we employed in situ hybridization and immunohistochemistry to map the expression of Met and its ligand, Hgf, through prenatal development of the mouse midbrain and hindbrain. Our results reveal a highly selective expression pattern of Met in the brainstem, including a subpopulation of neurons in cranial motor nuclei (nVII, nA and nXII), B6 subgroup of the dorsal raphe, Barrington's nucleus, and a small subset of neurons in the nucleus of solitary tract. In contrast to Met, neither full-length nor known splice variants of Hgf were localized in the prenatal brainstem. RT-PCR revealed Hgf expression in target tissues of Met-expressing brainstem neurons, suggesting that MET in these neurons may be activated by HGF from peripheral sources. Together, these data suggest that MET signaling may influence the development of neurons that are involved in central regulation of gastrointestinal function, tongue movement, swallowing, speech, stress and mood.

Indexed as

AnimalsBrain StemCranial NervesHepatocyte Growth FactorLateral VentriclesMiceMice, TransgenicNeuronsPineal GlandProto-Oncogene Proteins c-metRaphe NucleiHepatocyte Growth FactorHGF protein, mouseProto-Oncogene Proteins c-met

Identifiers

PMID23548689
PMCPMC3746026
OpenAlexW2000348834

What OpenQuestion holds

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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.