Evidence map›Paper›PMID 33265983›Full record

ArticleInternational journal of molecular sciences2020

2-Phenylethylamine (PEA) Ameliorates Corticosterone-Induced Depression-Like Phenotype via the BDNF/TrkB/CREB Signaling Pathway.

Young-Ju Lee, Hye Ryeong Kim, Chang Youn Lee, Sung-Ae Hyun, Moon Yi Ko, Byoung-Seok Lee, Dae Youn Hwang, Minhan Ka

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.6field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 67 citations in OpenAlex.

  1. Acetaminophen-induced acute liver injury abrogates the cytosine methylation pathway.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
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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

8 authors at 2 institutions in 1 country.

Young-Ju LeePharmacology and Drug Abuse Group, Convergence Toxicology Research Division, Korea Institute of Toxicology, KRICT, Daejeon 34114, Korea.
Hye Ryeong KimPharmacology and Drug Abuse Group, Convergence Toxicology Research Division, Korea Institute of Toxicology, KRICT, Daejeon 34114, Korea.
Chang Youn LeePharmacology and Drug Abuse Group, Convergence Toxicology Research Division, Korea Institute of Toxicology, KRICT, Daejeon 34114, Korea.
Sung-Ae HyunPharmacology and Drug Abuse Group, Convergence Toxicology Research Division, Korea Institute of Toxicology, KRICT, Daejeon 34114, Korea.
Moon Yi KoPharmacology and Drug Abuse Group, Convergence Toxicology Research Division, Korea Institute of Toxicology, KRICT, Daejeon 34114, Korea.
Byoung-Seok LeeDepartment of Advanced Toxicology Research, Korea Institute of Toxicology, KRICT, Daejeon 34114, Korea.
Dae Youn HwangDepartment of Biomaterials Science, College of Natural Resources and Life Science/Life and Industry Convergence Research Institute, Pusan National University, Miryang 50463, Korea.ORCID 0000-0002-5144-1725
Minhan KaPharmacology and Drug Abuse Group, Convergence Toxicology Research Division, Korea Institute of Toxicology, KRICT, Daejeon 34114, Korea.ORCID 0000-0003-2336-4184
Korea Institute of Toxicology · KRPusan National University · KR

Funding

Korea Institute of Toxicology KK-2005-02 and KK-1811-03Korea Technology and Information Promotion Agency for SMEs C0541691National Research Foundation of Korea NRF-2019R1A2C1009006
6 · The paper itself

Abstract

Depression is a serious medical illness that is one of the most prevalent psychiatric disorders. Corticosterone (CORT) increases depression-like behavior, with some effects on anxiety-like behavior. 2-Phenethylamine (PEA) is a monoamine alkaloid that acts as a central nervous system stimulant in humans. Here, we show that PEA exerts antidepressant effects by modulating the Brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/cAMP response element binding protein (CREB) signaling pathway in CORT-induced depression. To investigate the potential effects of PEA on CORT-induced depression, we first treated CORT (50 μM)-induced hippocampal neurons with 100 μM PEA for 24 h. We found that treatment with CORT altered dendritic spine architecture; however, treatment with PEA rescued dendritic spine formation via regulation of BDNF/TrkB/CREB signaling. Next, we used a mouse model of CORT-induced depression. Mice were treated with CORT (20 mg/kg) for 21 days, followed by assessments of a battery of depression-like behaviors. During the final four days of CORT exposure, the mice were treated with PEA (50 mg/kg). We found that CORT injection promoted depression-like behavior and significantly decreased BDNF and TrkB expression in the hippocampus. However, treatment with PEA significantly ameliorated the behavioral and biochemical changes induced by CORT. Our findings reveal that PEA exerts antidepressant effects by modulating the BDNF/TrkB/CREB signaling pathway in a mouse model of CORT-induced depression.

Indexed as

Signal TransductionAnimalsBehavior, AnimalBrain-Derived Neurotrophic FactorCorticosteroneCyclic AMP Response Element-Binding ProteinDendritic SpinesDepressionHippocampusMice, Inbred C57BLModels, BiologicalPhenethylaminesPhenotypeReceptor, trkBSynapsesBrain-Derived Neurotrophic FactorCorticosteroneCyclic AMP Response Element-Binding ProteinphenethylaminePhenethylaminesReceptor, trkB2-Phenylethylamine (PEA)BDNF/TrkB/CREB signalingcorticosteronedepressiondepression-like behavior

Identifiers

PMID33265983
PMCPMC7729630
OpenAlexW3107406382

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.