Evidence map›Paper›PMID 32705526›Full record

ArticleJournal of molecular neuroscience : MN2020

Effects of Single-Dose and Long-Term Ketamine Administration on Tau Phosphorylation-Related Enzymes GSK-3β, CDK5, PP2A, and PP2B in the Mouse Hippocampus.

Yanning Li, Gehua Wen, Runtao Ding, Xinghua Ren, Chenchen Jing, Lin Liu, Jun Yao, Guohua Zhang, Yan Lu, Baoman Li and 1 more

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 52% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. The role of Cdk5 in neurological disorders.Frontiers in cellular neuroscience · 2022
    Review
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

11 authors at 3 institutions in 1 country.

Yanning LiSchool of Forensic Medicine, China Medical University, Shenyang, People's Republic of China.
Gehua WenSchool of Forensic Medicine, China Medical University, Shenyang, People's Republic of China.
Runtao DingSchool of Forensic Medicine, China Medical University, Shenyang, People's Republic of China.
Xinghua RenSchool of Forensic Medicine, China Medical University, Shenyang, People's Republic of China.
Chenchen JingSchool of Basic Medicine, Gannan Medical University, Ganzhou, People's Republic of China.
Lin LiuSchool of Basic Medicine, Gannan Medical University, Ganzhou, People's Republic of China.
Jun YaoSchool of Forensic Medicine, China Medical University, Shenyang, People's Republic of China.
Guohua ZhangSchool of Forensic Medicine, China Medical University, Shenyang, People's Republic of China.
Yan LuKey Laboratory of Health Ministry in Congenital Malformation, The Affiliated Shengjing Hospital of China Medical University, Shenyang, People's Republic of China. luy1@sj-hospital.org.
Baoman LiSchool of Forensic Medicine, China Medical University, Shenyang, People's Republic of China. bmli@cmu.edu.cn.
Xu WuSchool of Forensic Medicine, China Medical University, Shenyang, People's Republic of China. xwu@cmu.edu.cn.ORCID https://orcid.org/0000-0003-3757-5767
China Medical University · CNGannan Medical University · CNCapital Medical University · CN

Funding

Key Scientific Research Project of Gannan Medical University ZD201828Liaoning Revitalization Talents Program XLYC1902059, XLYC1807137National Natural Science Foundation of China 81971794, 81960341, 81871852, 81671867
6 · The paper itself

Abstract

Ketamine is a recreational drug that causes emotional and cognitive impairments, but its specific mechanisms of action are still unclear. Recent evidence suggests that Tau protein phosphorylation and targeted delivery to the postsynaptic area are closely related to its neurotoxicity, and our recent studies have shown that long-term ketamine administration causes excessive Tau protein phosphorylation. However, the regulatory mechanism of Tau protein phosphorylation induced by ketamine has not been clarified. In the present study, we administered a single ketamine injection and long-term (6 months) ketamine injections in C57BL/6 mice, to investigate the effects of different doses of ketamine on the expression levels of Tau protein and its phosphorylation, the expression levels and activities of the related protein phosphokinases GSK-3β and CDK5, and the expression levels and activities of the related protein phosphatases PP2A and PP2B in the mouse hippocampus. Our results showed that both single-dose and long-term ketamine administration induced excessive phosphorylation of the Tau protein at ser202/thr205 and ser396. A single ketamine administration caused an increase in the activity of GSK-3β (at high doses) and a decrease in the activity of PP2A. On the other hand, long-term ketamine administration resulted in an increase in the activities of GSK-3β (at high doses) and CDK5, and a decrease in the activity of PP2A. Our results indicate that GSK-3β, CDK5, and PP2A may be involved in ketamine-induced Tau protein phosphorylation.

Indexed as

AnimalsCells, CulturedCyclin-Dependent Kinase 5Drug Administration ScheduleExcitatory Amino Acid AntagonistsGlycogen Synthase Kinase 3 betaHippocampusKetamineMaleMiceMice, Inbred C57BLPhosphorylationProtein Phosphatase 2tau ProteinsCdk5 protein, mouseCyclin-Dependent Kinase 5Excitatory Amino Acid AntagonistsGlycogen Synthase Kinase 3 betaKetamineProtein Phosphatase 2tau ProteinsCDK5GSK-3βKetaminePP2APP2BTau protein phosphorylation

Identifiers

PMID32705526
OpenAlexW3045280535

What OpenQuestion holds

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Read underepoch 390

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.