Evidence map›Paper›PMID 31920563›Full record

ArticleFrontiers in cellular neuroscience2019

Neuroprotective Effect of AM404 Against NMDA-Induced Hippocampal Excitotoxicity.

Soraya Wilke Saliba, Tiziana Bonifacino, Tsvetan Serchov, Giambattista Bonanno, Antônio Carlos Pinheiro de Oliveira, Bernd L Fiebich

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

8 citing papers in PubMed, 16 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

6 authors at 4 institutions in 3 countries.

Soraya Wilke SalibaNeuroimmunology and Neurochemistry Research Group, Department of Psychiatry and Psychotherapy, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Tiziana BonifacinoUnit of Pharmacology and Toxicology and Center of Excellence for Biomedical Research, Department of Pharmacy, School of Medical and Pharmaceutical Sciences, University of Genoa, Genoa, Italy.
Tsvetan SerchovLaboratory of Stereotaxy and Interventional Neuroscience, Department of Stereotactic and Functional Neurosurgery, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Giambattista BonannoUnit of Pharmacology and Toxicology and Center of Excellence for Biomedical Research, Department of Pharmacy, School of Medical and Pharmaceutical Sciences, University of Genoa, Genoa, Italy.
Antônio Carlos Pinheiro de OliveiraDepartment of Pharmacology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Bernd L FiebichNeuroimmunology and Neurochemistry Research Group, Department of Psychiatry and Psychotherapy, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
University of Freiburg · DEOspedale Policlinico San Martino · ITUniversidade Federal de Minas Gerais · BRUniversity of Genoa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Different studies have demonstrated that inflammation and alterations in glutamate neurotransmission are two events contributing to the pathophysiology of neurodegenerative or neurological disorders. There are evidences that N-arachidonoylphenolamine (AM404), a cannabinoid system modulator and paracetamol metabolite, modulates inflammation and exerts neuroprotective effects on Huntington's (HD) and Parkinson's diseases (PD), and ischemia. However, the effects of AM404 on the production of inflammatory mediators and excitotoxicity in brain tissue stimulated with N-methyl-D-aspartic acid (NMDA) are not elucidated. In this present study, we investigated the effects of AM404 on the production of inflammatory mediators and neuronal cell death induced by NMDA in organotypic hippocampal slices cultures (OHSC) using qPCR, western blot (WB), and immunohistochemistry. Moreover, to comprehend the mechanism of excitotoxicity, we evaluated the effects of AM404 on glutamate release in hippocampal synaptosomes and the NMDA-induced calcium responses in acute hippocampal slices. Our results showed that AM404 led to a significant decrease in cell death induced by NMDA, through a mechanism possibly involving the reduction of glutamate release and the calcium ions responses. Furthermore, it decreased the expression of the interleukin (IL)-1β. This study provides new significant insights about the anti-inflammatory and neuroprotection effects of AM404 on NMDA-induced excitotoxicity. To understand the effects of AM404 in these processes might contribute to the therapeutic potential of AM404 in diseases with involvement of neuroinflammation and neurodegeneration and might lead to a possible future treatment of neurodegenerative diseases.

Indexed as

AM404cannabinoid receptorexcitotoxicityhippocampusLPSneuroinflammationNMDAvanilloid receptor

Identifiers

PMID31920563
PMCPMC6932953
OpenAlexW2996304389

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.