Evidence map›Paper›PMID 26899575›Full record

ArticleMolecular neurobiology2017

Citalopram Ameliorates Synaptic Plasticity Deficits in Different Cognition-Associated Brain Regions Induced by Social Isolation in Middle-Aged Rats.

Wei-Gang Gong, Yan-Juan Wang, Hong Zhou, Xiao-Li Li, Feng Bai, Qing-Guo Ren, Zhi-Jun Zhang

Abstract read
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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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 48 citations in OpenAlex.

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  20. Spatial Training Ameliorates Long-Term Alzheimer's Disease-Like Pathological Deficits by Reducing NLRP3 Inflammasomes in PR5 Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    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

7 authors at 1 institution in 1 country.

Wei-Gang GongDepartment of Neuropsychiatry, Affiliated Zhong Da Hospital, School of Medicine, Southeast University, Nanjing, China.
Yan-Juan WangDepartment of Neuropsychiatry, Affiliated Zhong Da Hospital, School of Medicine, Southeast University, Nanjing, China.
Hong ZhouDepartment of Neuropsychiatry, Affiliated Zhong Da Hospital, School of Medicine, Southeast University, Nanjing, China.
Xiao-Li LiDepartment of Neuropsychiatry, Affiliated Zhong Da Hospital, School of Medicine, Southeast University, Nanjing, China.
Feng BaiDepartment of Neuropsychiatry, Affiliated Zhong Da Hospital, School of Medicine, Southeast University, Nanjing, China.
Qing-Guo RenDepartment of Neuropsychiatry, Affiliated Zhong Da Hospital, School of Medicine, Southeast University, Nanjing, China. renqingguo1976@163.com.
Zhi-Jun ZhangDepartment of Neuropsychiatry, Affiliated Zhong Da Hospital, School of Medicine, Southeast University, Nanjing, China.
Zhongda Hospital Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous experiments demonstrated that social isolation (SI) caused AD-like tau hyperphosphorylation and spatial memory deficits in middle-aged rats. However, the underlying mechanisms of SI-induced spatial memory deficits remain elusive. Middle-aged rats (10 months) were group or isolation reared for 8 weeks. Following the initial 4-week period of rearing, citalopram (10 mg/kg i.p.) was administered for 28 days. Then, pathophysiological changes were assessed by performing behavioral, biochemical, and pathological analyses. We found that SI could cause cognitive dysfunction and decrease synaptic protein (synaptophysin or PSD93) expression in different brain regions associated with cognition, such as the prefrontal cortex, dorsal hippocampus, ventral hippocampus, amygdala, and caudal putamen, but not in the entorhinal cortex or posterior cingulate. Citalopram could significantly improve learning and memory and partially restore synaptophysin or PSD93 expression in the prefrontal cortex, hippocampus, and amygdala in SI rats. Moreover, SI decreased the number of dendritic spines in the prefrontal cortex, dorsal hippocampus, and ventral hippocampus, which could be reversed by citalopram. Furthermore, SI reduced the levels of BDNF, serine-473-phosphorylated Akt (active form), and serine-9-phosphorylated GSK-3β (inactive form) with no significant changes in the levels of total GSK-3β and Akt in the dorsal hippocampus, but not in the posterior cingulate. Our results suggest that decreased synaptic plasticity in cognition-associated regions might contribute to SI-induced cognitive deficits, and citalopram could ameliorate these deficits by promoting synaptic plasticity mainly in the prefrontal cortex, dorsal hippocampus, and ventral hippocampus. The BDNF/Akt/GSK-3β pathway plays an important role in regulating synaptic plasticity in SI rats.

Indexed as

Social IsolationAge FactorsAnimalsBrainCitalopramCognitionCognition DisordersMaleMaze LearningMemory DisordersNeuronal PlasticityRatsRats, Sprague-DawleySelective Serotonin Reuptake InhibitorsSpatial MemoryCitalopramSelective Serotonin Reuptake InhibitorsAlzheimer’s diseaseCitalopramSocial isolationSpatial memorySynaptic plasticity

Identifiers

PMID26899575
OpenAlexW2275112773

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Registered trials

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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.