Evidence map›Paper›PMID 27012879›Full record

ArticleCNS neuroscience & therapeutics2016

HFS-Triggered AMPK Activation Phosphorylates GSK3β and Induces E-LTP in Rat Hippocampus In Vivo.

Dan-Fang Yu, Zu-Cheng Shen, Peng-Fei Wu, Xin-Lei Guan, Tao Chen, You Jin, Zhuang-Li Hu, Lan Ni, Fang Wang, Jian-Guo Chen and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Dan-Fang YuDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zu-Cheng ShenDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Peng-Fei WuDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xin-Lei GuanDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Tao ChenDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
You JinDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zhuang-Li HuDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Lan NiDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fang WangDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jian-Guo ChenDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Li-Hong LongDepartment of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ministry of Education of the People's Republic of China · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe AMP-activated protein kinase (AMPK) is a sensor of cellular energy and nutrient status, with substantial amount of cross talk with other signaling pathways, including its phosphorylation by Akt, PKA, and GSK3β.

aimsVarious signaling pathways and energy-consuming transport of glutamate receptors subunits are required in synaptic plasticity. However, it is unknown which energy sensors integrate the signaling pathways in these processes. In this article, we elucidated the role of AMPK activation and GSK3β phosphorylation after HFS during the inducement of early-phase long-term potentiation (E-LTP).

methodsSynaptic LTP in vivo was induced by high-frequency stimulation (HFS at 200 Hz at a 5-s interval). In addition, phosphorylation of AMPK and glycogen synthase kinase 3β (GSK3β) were measured using Western blotting. The amount of hippocampal AMP, ADP and ATP was measured by HPLC.

resultsWe showed that the phosphorylation of AMPK and GSK3β was significantly increased by HFS in vivo. HFS-induced AMPK activation occurred via increased (AMP + ADP)/ATP ratio and activation of Ca(2+) /calmodulin-dependent kinase kinase beta (CaMKKβ). Pharmacological inhibition of AMPK by compound C (CC) prevented HFS-induced inhibitory phosphorylation of GSK3β and the induction of LTP in dentate gyrus (DG) area in vivo.

conclusionsOur findings reveal that HFS-triggered AMPK activation phosphorylates GSK3β and induces E-LTP in vivo.

Indexed as

Adenine NucleotidesAMP-Activated Protein KinasesAnalysis of VarianceAnimalsChromatography, High Pressure LiquidDentate GyrusElectric StimulationEnzyme ActivationGene Expression RegulationGlycogen Synthase Kinase 3 betaLong-Term PotentiationMaleNeuronsPhosphorylationRatsRats, Sprague-DawleyAdenine NucleotidesAMP-Activated Protein KinasesGlycogen Synthase Kinase 3 betaAMP-activated protein kinaseE-LTPGlycogen synthase kinase 3βHigh-frequency stimulation

Identifiers

PMID27012879
PMCPMC6492836
OpenAlexW2307747194

What OpenQuestion holds

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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.