Evidence map›Paper›PMID 37124348›Full record

ReviewBiological psychiatry global open science2023

Dysfunction of Glutamatergic Synaptic Transmission in Depression: Focus on AMPA Receptor Trafficking.

Jin-Gang He, Hai-Yun Zhou, Fang Wang, Jian-Guo Chen

Open access · goldAbstract readReview
In one paragraph

Review in Biological psychiatry global open science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Advancing past ketamine: emerging glutamatergic compounds for the treatment of depression.European archives of psychiatry and clinical neuroscience · 2025
    Review
  11. Ketamine Reverses Chronic Stress-Induced Behavioral Changes via the Expression of CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  12. Article
  13. Review
  14. Genome-wide methylome-based molecular pathologies associated with depression and suicide.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  15. Review
  16. The role of astrocytes in depression, its prevention, and treatment by targeting astroglial gliotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  17. Article
  18. New Light on Prions: Putative Role of PrPInternational journal of molecular sciences · 2024
    Review
  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

4 authors at 1 institution in 1 country.

Jin-Gang HeDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hai-Yun ZhouDepartment of Pharmacy, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fang WangDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jian-Guo ChenDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacological and anatomical evidence suggests that abnormal glutamatergic neurotransmission may be associated with the pathophysiology of depression. Compounds that act as NMDA receptor antagonists may be a potential treatment for depression, notably the rapid-acting agent ketamine. The rapid-acting and sustained antidepressant effects of ketamine rely on the activation of AMPA receptors (AMPARs). As the key elements of fast excitatory neurotransmission in the brain, AMPARs are crucially involved in synaptic plasticity and memory. Recent efforts have been directed toward investigating the bidirectional dysregulation of AMPAR-mediated synaptic transmission in depression. Here, we summarize the published evidence relevant to the dysfunction of AMPAR in stress conditions and review the recent progress toward the understanding of the involvement of AMPAR trafficking in the pathophysiology of depression, focusing on the roles of AMPAR auxiliary subunits, key AMPAR-interacting proteins, and posttranslational regulation of AMPARs. We also discuss new prospects for the development of improved therapeutics for depression.

Indexed as

AMPA receptorDepressionReceptor traffickingStressSynaptic transmission

Identifiers

PMID37124348
PMCPMC10140449
OpenAlexW4220943308

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.