Evidence map›Paper›PMID 30405339›Full record

ArticleFrontiers in neuroscience2018

Liraglutide Activates mTORC1 Signaling and AMPA Receptors in Rat Hippocampal Neurons Under Toxic Conditions.

Sung Woo Park, Rodrigo B Mansur, Yena Lee, Jae-Hon Lee, Mi Kyoung Seo, Ah Jeong Choi, Roger S McIntyre, Jung Goo Lee

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 29% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

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  4. Establishment of a Depression Model Using Dexamethasone-treated Three-dimensional Cultured Rat Cortical Cells.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025
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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 3 institutions in 2 countries.

Sung Woo ParkPaik Institute for Clinical Research, Inje University, Busan, South Korea.
Rodrigo B MansurMood Disorders Psychopharmacology Unit, University Health Network, University of Toronto, Toronto, ON, Canada.
Yena LeeMood Disorders Psychopharmacology Unit, University Health Network, University of Toronto, Toronto, ON, Canada.
Jae-Hon LeeDepartment of Psychiatry, National Rehabilitation Center, Seoul, South Korea.
Mi Kyoung SeoPaik Institute for Clinical Research, Inje University, Busan, South Korea.
Ah Jeong ChoiPaik Institute for Clinical Research, Inje University, Busan, South Korea.
Roger S McIntyreMood Disorders Psychopharmacology Unit, University Health Network, University of Toronto, Toronto, ON, Canada.
Jung Goo LeePaik Institute for Clinical Research, Inje University, Busan, South Korea.
Inje University · KRUniversity Health Network · CAInje University Busan Paik Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to determine whether treatment with liraglutide, a glucagon-like peptide 1 (GLP-1) receptor agonist, would alter mammalian target of rapamycin complex 1 (mTORC1) signaling and/or α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor activity under dexamethasone-induced toxic conditions. Western blot analyses were performed to assess changes in mTORC1-mediated proteins, brain-derived neurotrophic factor (BDNF), and various synaptic proteins (PSD-95, synapsin I, and GluA1) in rat hippocampal cultures under toxic conditions induced by dexamethasone, which causes hippocampal cell death. Hippocampal dendritic outgrowth and spine formation were measured using immunostaining procedures. Dexamethasone significantly decreased the phosphorylation levels of mTORC1 as well as its downstream proteins. However, treatment with liraglutide prevented these reductions and significantly increased BDNF expression. The increase in BDNF expression was completely blocked by rapamycin and 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX). Liraglutide also recovered dexamethasone-induced decreases in the total length of hippocampal dendrites and reductions in spine density in a concentration-dependent manner. However, the positive effects of liraglutide on neural plasticity were abolished by the blockade of mTORC1 signaling and AMPA receptors. Furthermore, liraglutide significantly increased the expression levels of PSD-95, synapsin I, and GluA1, whereas rapamycin and NBQX blocked these effects. The present study demonstrated that liraglutide activated mTORC1 signaling and AMPA receptor activity as well as increased dendritic outgrowth, spine density, and synaptic proteins under toxic conditions in rat primary hippocampal neurons. These findings suggest that GLP-1 receptor (GLP-1R) activation by liraglutide may affect neuroplasticity through mTORC1 and AMPA receptors.

Indexed as

glucagon-like peptide 1 receptorliraglutidemammalian target of rapamycin complex 1 signalingneuroplasticitytoxic conditionα-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor

Identifiers

PMID30405339
PMCPMC6205986
OpenAlexW2896427313

What OpenQuestion holds

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LicenceCC BY
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.