Evidence map›Paper›PMID 37715015›Full record

ArticlePsychopharmacology2024

Simvastatin ameliorates synaptic plasticity impairment in chronic mild stress-induced depressed mice by modulating hippocampal NMDA receptor.

Xu-Ben Yu, Kai-Long Zhong, Chuang Chen, Jing Fu, Fang Chen, Hong-Min Zhou, Xiu-Hua Zhang, Kwonseop Kim, Jing-Ye Pan

Abstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. 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

9 authors at 4 institutions in 2 countries.

Xu-Ben Yu *School of Pharmacy, Chonnam National University, Gwangju, South Korea. yuxuben@126.com.ORCID http://orcid.org/0000-0003-1897-4519
Kai-Long Zhong *Department of Pharmacy, Xiamen Clinical Research Center for Cancer Therapy, Zhongshan Hospital (Xiamen), Fudan University, Xiamen, 361015, People's Republic of China.
Chuang ChenSchool of Pharmacy, Wenzhou Medical University, Wenzhou, 325035, People's Republic of China.
Jing FuSchool of Pharmacy, Wenzhou Medical University, Wenzhou, 325035, People's Republic of China.
Fang ChenDepartment of Pharmacy, The First Affiliated Hospital of Xiamen University, Xiamen, 361005, People's Republic of China.
Hong-Min ZhouIntensive Care Unit, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, People's Republic of China.
Xiu-Hua ZhangClinical Research Center, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, People's Republic of China.
Kwonseop KimSchool of Pharmacy, Chonnam National University, Gwangju, South Korea. koskim@chonnam.ac.kr.
Jing-Ye PanIntensive Care Unit, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, People's Republic of China. panjingye@wzhospital.cn.
Wenzhou Medical University · CNChonnam National University · KRFirst Affiliated Hospital of Xiamen University · CNFudan University · CN

Funding

National Natural Science Foundation of China 82104145Natural Science Foundation of Zhejiang Province LQ20H310003
6 · The paper itself

Abstract

backgroundIn our previous study, we showed simvastatin exerts an antidepressant effect and inhibits neuroinflammation. Given the role of synaptic impairment in depression development, we investigate the effect of simvastatin on synaptic plasticity in depression and the related mechanisms.

methodsElectrophysiological analysis, Golgi staining, and transmission electron microscope were performed to analyze the effect of simvastatin on synaptic impairment in depression. In addition, the localization and reactivity of N-methyl-D-aspartate receptor (NMDAR) subunits and the downstream signaling were investigated to explore the mechanism of simvastatin's effect on synaptic plasticity.

resultsSimvastatin ameliorated the reduction of the magnitude of long-term potentiation (LTP) in Schaffer collateral-CA1, restored hippocampal dendritic spine density loss, improved the number of spine synapses, reversed the reduction in BrdU-positive cells in chronic mild stress (CMS)-induced depressed mice, and ameliorated NMDA-induced neurotoxicity in hippocampal neurons. Dysfunction of NMDAR activity in the hippocampus is associated with depression. Simvastatin treatment reversed the surface expression and phosphorylation changes of NMDAR subunits in NMDA-treated hippocampal neurons and depressed mice. In addition, simvastatin further increased the levels of mature BDNF, activating TrkB-Akt-mTOR signaling, which is critical for synaptic plasticity.

conclusionsThese findings suggest that simvastatin can improve the dysfunction of NMDAR and ameliorate hippocampal synaptic plasticity impairment in depressed mice.

Indexed as

N-MethylaspartateReceptors, N-Methyl-D-AspartateAnimalsHippocampusLong-Term PotentiationMiceNeuronal PlasticitySimvastatinSynapsesSynaptic TransmissionN-MethylaspartateReceptors, N-Methyl-D-AspartateSimvastatinDepressionNMDA receptorSimvastatinSynaptic plasticity

Identifiers

PMID37715015
OpenAlexW4386760086

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.