Evidence map›Paper›PMID 21839100›Full record

ArticleNeuropharmacology2011

Chronic valproate treatment blocks D2-like receptor-mediated brain signaling via arachidonic acid in rats.

Epolia Ramadan, Mireille Basselin, Ameer Y Taha, Yewon Cheon, Lisa Chang, Mei Chen, Stanley I Rapoport

Abstract read
In one paragraph

Article in Neuropharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The Role of CaMKII and ERK Signaling in Addiction.International journal of molecular sciences · 2021
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Chronic valproate attenuates some, but not all, facets of mania-like behaviour in mice.The international journal of neuropsychopharmacology · 2013
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. The synthesis and in vivo pharmacokinetics of fluorinated arachidonic acid: implications for imaging neuroinflammation.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2012
    Article
  17. Review
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

7 authors at 3 institutions in 1 country.

Epolia RamadanBrain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA. ramadanir@mail.nih.gov
Mireille Basselin
Ameer Y Taha
Yewon Cheon
Lisa Chang
Mei Chen
Stanley I Rapoport
National Institute on Aging · USInstitute on Aging · USNational Institutes of Health · US

Funding

Psychoactive Drug Effects on Brain Arachidonic Acid Signaling and Metabolism ZIAAG000150 · NIA · NATIONAL INSTITUTE ON AGING · PI RAPOPORT, STANLEY I. · 2009 to 2016
$4.9M
Imaging Brain Signal Transduction via Arachidonic and Docosahexaenoic AcidsZIAAG000134 · NIA · NATIONAL INSTITUTE ON AGING · PI RAPOPORT, STANLEY I. · 2009 to 2015
$3.3M
THE NERVOUS SYSTEM IN RELATION TO FUNCTION, AGING, AND DISEASEZ01AG000134 · NIA · NATIONAL INSTITUTE ON AGING · PI RAPOPORT, STANLEY I. · 1985 to 2008
$1.2M
Anti-Bipolar Disorder Agents and Brain Arachidonic Acid SignalingZ01AG000150 · NIA · NATIONAL INSTITUTE ON AGING · PI RAPOPORT, STANLEY I. · 2008 to 2008
$270k
Intramural NIH HHS Z01 AG000134Intramural NIH HHS Z01 AG000150Intramural NIH HHS Z99 AG999999Intramural NIH HHS ZIA AG000134NIA NIH HHS R99 AG999999
6 · The paper itself

Abstract

BACKGROUND AND

objectiveHyperdopaminergic signaling and an upregulated brain arachidonic acid (AA) cascade may contribute to bipolar disorder (BD). Lithium and carbamazepine, FDA-approved for the treatment of BD, attenuate brain dopaminergic D(2)-like (D(2), D(3), and D(4)) receptor signaling involving AA when given chronically to awake rats. We hypothesized that valproate (VPA), with mood-stabilizing properties, would also reduce D(2)-like-mediated signaling via AA.

methodsAn acute dose of quinpirole (1 mg/kg) or saline was administered to unanesthetized rats that had been treated for 30 days with a therapeutically relevant dose of VPA (200 mg/kg/day) or vehicle. Regional brain AA incorporation coefficients, k*, and incorporation rates, J(in), markers of AA signaling and metabolism, were measured by quantitative autoradiography after intravenous [1-(14)C]AA infusion. Whole brain concentrations of prostaglandin (PG)E(2) and thromboxane (TX)B(2) also were measured.

resultsQuinpirole compared to saline significantly increased k* in 40 of 83 brain regions, and increased brain concentrations of PGE(2) in chronic vehicle-treated rats. VPA treatment by itself reduced concentrations of plasma unesterified AA and whole brain PGE(2) and TXB(2), and blocked the quinpirole-induced increments in k* and PGE(2).

conclusionThese results further provide evidence that mood stabilizers downregulate brain dopaminergic D(2)-like receptor signaling involving AA.

Indexed as

Analysis of VarianceAnimalsAntimanic AgentsArachidonic AcidAutoradiographyBrainCarbon RadioisotopesDinoprostoneDopamine AgonistsDopamine AntagonistsMaleRatsRats, Inbred F344Receptors, Dopamine D2Signal TransductionThromboxane B2Antimanic AgentsArachidonic AcidCarbon RadioisotopesDinoprostoneDopamine AgonistsDopamine AntagonistsReceptors, Dopamine D2Thromboxane B2Valproic Acid

Identifiers

PMID21839100
PMCPMC3190603
OpenAlexW1989285598

What OpenQuestion holds

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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.