Evidence map›Paper›PMID 29793154›Full record

ArticleNeuropharmacology2018

Juvenile treatment with mGluR2/3 agonist prevents schizophrenia-like phenotypes in adult by acting through GSK3β.

Bo Xing, Genie Han, Min-Juan Wang, Melissa A Snyder, Wen-Jun Gao

Abstract read
In one paragraph

Article in Neuropharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Distinct Roles for Prefrontal Dopamine D1 and D2 Neurons in Social Hierarchy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  6. Article
  7. Review
  8. Cognitive Deficit in Schizophrenia: From Etiology to Novel Treatments.International journal of molecular sciences · 2021
    Review
  9. Review
  10. Review
  11. Review
  12. 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

5 authors at 1 institution in 1 country.

Bo XingDepartment of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, 19129, PA, USA.
Genie HanDepartment of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, 19129, PA, USA.
Min-Juan WangDepartment of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, 19129, PA, USA.
Melissa A SnyderDepartment of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, 19129, PA, USA.
Wen-Jun GaoDepartment of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, 19129, PA, USA. Electronic address: wg38@drexel.edu.
Drexel University · US

Funding

Development of NMDAR hypofunction and cognitive deficitsR01MH085666 · NIMH · DREXEL UNIVERSITY · PI GAO, WEN-JUN · 2009 to 2018
$3.8M
Role of prefrontal cortical dopamine in aggressionR21MH110678 · NIMH · DREXEL UNIVERSITY · PI GAO, WEN-JUN · 2016 to 2017
$425k
NIMH NIH HHS R01 MH085666NIMH NIH HHS R21 MH110678
6 · The paper itself

Abstract

Prodromal memory deficits represent an important marker for the development of schizophrenia (SZ), in which glutamatergic hypofunction occurs in the prefrontal cortex (PFC). The mGluR2/3 agonist LY379268 (LY37) attenuates excitatory N-methyl-D-aspartate receptor (NMDAR)-induced neurotoxicity, a central pathological characteristic of glutamatergic hypofunction. We therefore hypothesized that early treatment with LY37 would rescue cognitive deficits and confer benefits for SZ-like behaviors in adults. To test this, we assessed whether early intervention with LY37 would improve learning outcomes in the Morris Water Maze for rats prenatally exposed to methylazoxymethanol acetate (MAM), a neurodevelopmental SZ model. We found that a medium dose of LY37 prevents learning deficits in MAM rats. These effects were mediated through postsynaptic mGluR2/3 via improving GluN2B-NMDAR function by inhibiting glycogen synthase kinase-3β (GSK3β). Furthermore, dendritic spine loss and learning and memory deficits observed in adult MAM rats were restored by juvenile LY37 treatment, which did not change prefrontal neuronal excitability and glutamatergic synaptic transmission in adult normal rats. Our results provide a mechanism for mGluR2/3 agonists against NMDAR hypofunction, which may prove to be beneficial in the prophylactic treatment of SZ.

Indexed as

Amino AcidsAnimalsAntipsychotic AgentsBridged Bicyclo Compounds, HeterocyclicDendritic SpinesDisease Models, AnimalExcitatory Amino Acid AgonistsFemaleGlycogen Synthase Kinase 3 betaLearning DisabilitiesMethylazoxymethanol AcetatePrefrontal CortexPregnancyPrenatal Exposure Delayed EffectsRats, Sprague-DawleyReceptors, Metabotropic GlutamateAmino AcidsAntipsychotic AgentsBridged Bicyclo Compounds, HeterocyclicExcitatory Amino Acid AgonistsGlycogen Synthase Kinase 3 betaLY 379268metabotropic glutamate receptor 2metabotropic glutamate receptor 3Methylazoxymethanol AcetateReceptors, Metabotropic GlutamateAnimal modelmGluR2/3 agonistNeurodevelopmentNMDA receptorPrefrontal cortexSchizophrenia

Identifiers

PMID29793154
PMCPMC6050107
OpenAlexW2803303422

What OpenQuestion holds

Textmetadata
LicenceTDM
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.