Evidence map›Paper›PMID 15800181›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Chronic antidepressants reduce depolarization-evoked glutamate release and protein interactions favoring formation of SNARE complex in hippocampus.

Giambattista Bonanno, Roberto Giambelli, Luca Raiteri, Ettore Tiraboschi, Simona Zappettini, Laura Musazzi, Maurizio Raiteri, Giorgio Racagni, Maurizio Popoli

Registry-linked trialOpen access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04234776 (Intramuscular Ketamine Versus Escitalopram and Aripiprazole in Acute and Maintenance Treatment of Patients With Treatment-resistant Depression), which is not on this map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.8field-weighted citation impact, top 4% 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.

NCT04234776 phase4unknown statusnot on this mapstarted 2018, after this paper: background citation

Intramuscular Ketamine Versus Escitalopram and Aripiprazole in Acute and Maintenance Treatment of Patients With Treatment-resistant Depression

TypeinterventionalSponsorUniversity of Sao PauloRan2018 to 2021Enrolled88ConditionsDepressive DisorderArmsKetamine, Cognition, Suicide risk, Depression thoughts, Quality of life and disability
3 · Its place in the literature

Who cites it

76 citing papers in PubMed, 230 citations in OpenAlex.

  1. Trial
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  8. eLife · 2023
    Article
  9. Article
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  16. The Depolarization-Evoked, CaFrontiers in pharmacology · 2021
    Article
  17. Review
  18. Review
  19. Article
  20. Review

16 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Giambattista BonannoSection of Pharmacology and Toxicology, Department of Experimental Medicine, and Center of Excellence for Biomedical Research, University of Genoa, 16148 Genoa, Italy.
Roberto Giambelli
Luca Raiteri
Ettore Tiraboschi
Simona Zappettini
Laura Musazzi
Maurizio Raiteri
Giorgio Racagni
Maurizio Popoli
University of Genoa · ITUniversity of Milan · ITCentro San Giovanni di Dio Fatebenefratelli · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutamate neurotransmission was recently implicated in the action of stress and in antidepressant mechanisms. We report that chronic (not acute) treatment with three antidepressants with different primary mechanisms (fluoxetine, reboxetine, and desipramine) markedly reduced depolarization-evoked release of glutamate, stimulated by 15 or 25 mm KCl, but not release of GABA. Endogenous glutamate and GABA release was measured in superfused synaptosomes, freshly prepared from hippocampus of drug-treated rats. Interestingly, treatment with the three drugs only barely changed the release of glutamate (and of GABA) induced by ionomycin. In synaptic membranes of chronically treated rats we found a marked reduction in the protein-protein interaction between syntaxin 1 and Thr286-phosphorylated alphaCaM kinase II (alpha-calcium/calmodulin-dependent protein kinase II) (an interaction previously proposed to promote neurotransmitter release) and a marked increase in the interaction between syntaxin 1 and Munc-18 (an interaction proposed to reduce neurotransmitter release). Furthermore, we found a selective reduction in the expression level of the three proteins forming the core SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complex. These findings suggest that antidepressants work by stabilizing glutamate neurotransmission in the hippocampus and that they may represent a useful tool for the study of relationship between functional and molecular processes in nerve terminals.

Indexed as

AnimalsAntidepressive AgentsBlotting, WesternCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Dose-Response Relationship, DrugDrug Administration ScheduleDrug Interactionsgamma-Aminobutyric AcidGlutamic AcidHippocampusImmunoprecipitationIonomycinIonophoresMaleAntidepressive AgentsCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, ratgamma-Aminobutyric AcidGlutamic AcidIonomycinIonophoresMunc18 ProteinsPotassium ChlorideSNARE ProteinsSyntaxin 1Threonine

Identifiers

PMID15800181
PMCPMC6724889
OpenAlexW2131812309

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.