Evidence map›Paper›PMID 27578017›Full record

ArticleMolecular neurobiology2017

Alleviation of N-Methyl-D-Aspartate Receptor-Dependent Long-Term Depression via Regulation of the Glycogen Synthase Kinase-3β Pathway in the Amygdala of a Valproic Acid-Induced Animal Model of Autism.

Han-Fang Wu, Po See Chen, Yi-Ju Chen, Chi-Wei Lee, I-Tuan Chen, Hui-Ching Lin

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Exploring key genes and pathways associated with sex differences in autism spectrum disorder: integrated bioinformatic analysis.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Generational synaptic functions of GABAJournal of biomedical science · 2022
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Valproate ExposureFrontiers in physiology · 2019
    Article
  19. Review
  20. Molecular neurobiology · 2018
    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

6 authors at 3 institutions in 1 country.

Han-Fang WuDepartment and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, 11221, Taiwan.
Po See ChenDepartment of Psychiatry, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Yi-Ju ChenDepartment and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, 11221, Taiwan.
Chi-Wei LeeDepartment and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, 11221, Taiwan.
I-Tuan ChenDepartment and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, 11221, Taiwan.
Hui-Ching LinDepartment and Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei, 11221, Taiwan. hclin7@ym.edu.tw.
National Yang Ming Chiao Tung University · TWNational Cheng Kung University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The amygdala plays crucial roles in socio-emotional behavior and cognition, both of which are abnormal in autism spectrum disorder (ASD). Valproic acid (VPA)-exposed rat offspring have demonstrated ASD phenotypes and amygdala excitatory/inhibitory imbalance. However, the role of glutamatergic synapses in this imbalance remains unclear. In this study, we used a VPA-induced ASD-like model to assess glutamatergic synapse-dependent long-term depression (LTD) and depotentiation (DPT) in the amygdala. We first confirmed that the VPA-exposed offspring exhibited sociability deficits, anxiety, depression-like behavior, and abnormal nociception thresholds. Then, electrophysiological examination showed a significantly decreased paired-pulse ratio in the amygdala. In addition, both NMDA-dependent LTD and DPT were absent from the amygdala. Furthermore, we found that the levels of glycogen synthase kinase3β (GSK-3β) phosphorylation and β-catenin were significantly higher in the amygdala of the experimental animals than in the controls. Local infusion of phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin into the amygdala reversed the increased phosphorylation level and impaired social behavior. Taken together, the results suggested that NMDA receptor-related synaptic plasticity is dysfunctional in VPA-exposed offspring. In addition, GSK-3β in the amygdala is critical for synaptic plasticity at the glutamatergic synapses and is related to social behavior. Its role in the underlying mechanism of ASD merits further investigation.

Indexed as

Neuronal PlasticityAnimalsAutistic DisorderDepressionDisease Models, AnimalEnzyme InhibitorsGlycogen Synthase Kinase 3 betaRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateSocial BehaviorValproic AcidEnzyme InhibitorsGlycogen Synthase Kinase 3 betaReceptors, N-Methyl-D-AspartateValproic AcidAmygdalaAutism spectrum disorderGSK-3βLong-term depressionN-Methyl-D-aspartate receptorValproic acid

Identifiers

PMID27578017
OpenAlexW2511577082

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.