Evidence map›Paper›PMID 34532457›Full record

ArticleAnnals of translational medicine2021

Effects of N-Methyl-D-aspartate receptor (NMDAR) and Ca

Yuxi Zhang, Li Ren, Su Min, Feng Lv, Jian Yu

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Article
  5. Article
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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 2 institutions in 1 country.

Yuxi ZhangDepartment of Anesthesiology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Li RenDepartment of Anesthesiology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Su MinDepartment of Anesthesiology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Feng LvDepartment of Anesthesiology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jian YuDepartment of Anesthesiology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
First Affiliated Hospital of Chongqing Medical University · CNChongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWith the development of modified electroshock therapy (MECT), it has become necessary to increase the electric quantity in order to achieve a good antidepressant effect, but this increase will lead to more serious learning and memory impairment. The purpose of this study was to investigate the intrinsic mechanism of cognitive impairment induced by high-energy electroconvulsive shock (MECS, an animal model of MECT).

methodsRats were randomly divided into 6 groups: control (C, n=6), M0, M60, M120, M180, and M240 groups (MECS at 0, 60, 120, 180, and 240 mC stimulation intensity after 80 mg/kg propofol, with 12 rats in each group). Their depression-like behavior and learning and memory ability were evaluated by sucrose preference test (SPT), open field test (OFT), and Morris water maze test (MWM). The expression of phospho-NMDA receptor 1 (GluN1), GluN2A, GluN2B, Ca

resultsThe chronic unpredictable mild stresses (CUMS) procedure successfully induced depression-like behavior in rats, which was improved in varying degrees after MECS. The results showed that the expression of GluN1, GluN2A, GluN2B, and PSD-95 decreased with the increase of charge, while p-T305-CaMKII increased, which led to the deterioration of learning and memory ability, but the expression change of CaMKIIα was not statistically significant.

conclusionsIncrease in the MECS charge adjusts the synaptic plasticity by changing the binding amount of CaMKIIα and its subunit GluN2B and the level of CaMKII autophosphorylation, thereby impairing learning and memory functions.

Indexed as

Depressionelectroconvulsive therapyN-Methyl-D-aspartate receptor (NMDAR)synaptic plasticity

Identifiers

PMID34532457
PMCPMC8422109
OpenAlexW3197463377

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.