Evidence map›Paper›PMID 17093977›Full record

ArticlePsychopharmacology2007

Chronic fluoxetine increases cytosolic phospholipase A(2) activity and arachidonic acid turnover in brain phospholipids of the unanesthetized rat.

Ho-Joo Lee, Jagadeesh S Rao, Renee N Ertley, Lisa Chang, Stanley I Rapoport, Richard P Bazinet

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 42 citations in OpenAlex.

  1. Fluoxetine Arrests Growth of the Model DiatomFrontiers in microbiology · 2020
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  19. Imaging elevated brain arachidonic acid signaling in unanesthetized serotonin transporter (5-HTT)-deficient mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2009
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Ho-Joo LeeBrain Physiology and Metabolism Section National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA.
Jagadeesh S Rao
Renee N Ertley
Lisa Chang
Stanley I Rapoport
Richard P Bazinet
Institute on Aging · USNational Institute on Aging · USNational Institutes of Health · US

Funding

Molecular Mechanisms of Action of Lithium and Other Anti-Bipolar Disorder AgentsZ01AG000145 · NIA · NATIONAL INSTITUTE ON AGING · PI RAPOPORT, STANLEY I. · 2001 to 2008
$1.2M
Molecular Mechanisms of Action of Lithium and Other Anti-Bipolar Disorder AgentsZIAAG000145 · NIA · NATIONAL INSTITUTE ON AGING · PI RAPOPORT, STANLEY I. · 2009 to 2010
$624k
Intramural NIH HHS
6 · The paper itself

Abstract

rationaleFluoxetine is used to treat unipolar depression and is thought to act by increasing the concentration of serotonin (5-HT) in the synaptic cleft, leading to increased serotonin signaling. The 5-HT(2A/2C) receptor subtypes are coupled to a phospholipase A(2) (PLA(2)). We hypothesized that chronic fluoxetine would increase the brain activity of PLA(2) and the turnover rate of arachidonic acid (AA) in phospholipids of the unanesthetized rat. MATERIALS AND

methodsTo test this hypothesis, rats were administered fluoxetine (10 mg/kg) or vehicle intraperitoneally daily for 21 days. In the unanesthetized rat, [1-(14)C]AA was infused intravenously and arterial blood plasma was sampled until the animal was killed at 5 min and its brain was subjected to chemical, radiotracer, or enzyme analysis.

resultsUsing equations from our fatty acid model, we found that chronic fluoxetine compared with vehicle increased the turnover rate of AA within several brain phospholipids by 75-86%. The activity and protein levels of brain cytosolic PLA(2) (cPLA(2)) but not of secretory or calcium-independent PLA(2) were increased in rats administered fluoxetine. In a separate group of animals that received chronic fluoxetine followed by a 3-day saline washout, the turnover of AA and activity and protein levels of cPLA(2) were not significantly different from controls. The protein levels of cyclooxygenases 1 and 2 as well as the concentration of prostaglandin E(2) in rats chronically administered fluoxetine did not differ significantly from controls.

conclusionThe results support the hypothesis that fluoxetine increases the cPLA(2)-mediated turnover of AA within brain phospholipids.

Indexed as

AnimalsAntidepressive Agents, Second-GenerationArachidonic AcidBrainCytosolFluoxetineFluvoxamineFrontal LobeInjections, IntraperitonealMalePhospholipases APhospholipidsRatsRats, Inbred F344Receptor, Serotonin, 5-HT2AReceptor, Serotonin, 5-HT2CAntidepressive Agents, Second-GenerationArachidonic AcidFluoxetineFluvoxaminePhospholipases APhospholipidsReceptor, Serotonin, 5-HT2AReceptor, Serotonin, 5-HT2CSelective Serotonin Reuptake Inhibitors

Identifiers

PMID17093977
OpenAlexW2034108687

What OpenQuestion holds

Textmetadata
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.