Evidence map›Paper›PMID 35721318›Full record

ArticleFrontiers in molecular neuroscience2022

Transactivation of TrkB Receptors by Oxytocin and Its G Protein-Coupled Receptor.

Mariela Mitre, Khalil Saadipour, Kevin Williams, Latika Khatri, Robert C Froemke, Moses V Chao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Confronting the loss of trophic support.Frontiers in molecular neuroscience · 2023
    Article
  11. Review
  12. FreshFrontiers in pharmacology · 2023
    Article
  13. 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

6 authors at 4 institutions in 1 country.

Mariela MitreDepartments of Cell Biology, Neuroscience & Physiology, and Psychiatry, Skirball Institute for Biomolecular Medicine, New York, NY, United States.
Khalil SaadipourDepartments of Cell Biology, Neuroscience & Physiology, and Psychiatry, Skirball Institute for Biomolecular Medicine, New York, NY, United States.
Kevin WilliamsDepartments of Biology and Psychology, University of Georgia, Athens, GA, United States.
Latika KhatriDepartments of Cell Biology, Neuroscience & Physiology, and Psychiatry, Skirball Institute for Biomolecular Medicine, New York, NY, United States.
Robert C FroemkeDepartments of Cell Biology, Neuroscience & Physiology, and Psychiatry, Skirball Institute for Biomolecular Medicine, New York, NY, United States.
Moses V ChaoDepartments of Cell Biology, Neuroscience & Physiology, and Psychiatry, Skirball Institute for Biomolecular Medicine, New York, NY, United States.
Institute for Molecular Medicine · USNYU Langone Health · USNew York University · USUniversity of Georgia · US

Funding

U19 Supplement 2023-FroemkeU19NS107616 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RICHARD W TSIEN · 2018 to 2026
$36.4M
Targets of Oxytocin Receptor SignalingR01MH119136 · NIMH · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CHAO, MOSES VICTOR · 2019 to 2023
$2.3M
NIMH NIH HHS R01 MH119136NINDS NIH HHS U19 NS107616
6 · The paper itself

Abstract

Brain-derived Neurotrophic Factor (BDNF) binds to the TrkB tyrosine kinase receptor, which dictates the sensitivity of neurons to BDNF. A unique feature of TrkB is the ability to be activated by small molecules in a process called transactivation. Here we report that the brain neuropeptide oxytocin increases BDNF TrkB activity in primary cortical neurons and in the mammalian neocortex during postnatal development. Oxytocin produces its effects through a G protein-coupled receptor (GPCR), however, the receptor signaling events that account for its actions have not been fully defined. We find oxytocin rapidly transactivates TrkB receptors in bath application of acute brain slices of 2-week-old mice and in primary cortical culture by increasing TrkB receptor tyrosine phosphorylation. The effects of oxytocin signaling could be distinguished from the related vasopressin receptor. The transactivation of TrkB receptors by oxytocin enhances the clustering of gephyrin, a scaffold protein responsible to coordinate inhibitory responses. Because oxytocin displays pro-social functions in maternal care, cognition, and social attachment, it is currently a focus of therapeutic strategies in autism spectrum disorders. Interestingly, oxytocin and BDNF are both implicated in the pathophysiology of depression, schizophrenia, anxiety, and cognition. These results imply that oxytocin may rely upon crosstalk with BDNF signaling to facilitate its actions through receptor transactivation.

Indexed as

neurotrophinoxytocinreceptor tyrosine kinase receptorstransactivationtrophic

Identifiers

PMID35721318
PMCPMC9201241
OpenAlexW4281803068

What Socratic 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 Socratic graph.