Evidence map›Paper›PMID 18461450›Full record

ArticleNeurochemical research2008

Chronic administration of valproic acid reduces brain NMDA signaling via arachidonic acid in unanesthetized rats.

Mireille Basselin, Lisa Chang, Mei Chen, Jane M Bell, Stanley I Rapoport

Open access · greenAbstract read
In one paragraph

Article in Neurochemical research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
8.4field-weighted citation impact, top 3% 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, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. NMDA Receptors: Next therapeutic targets for Tinnitus?Biochemistry and biophysics reports · 2025
    Review
  5. Review
  6. Article
  7. Neuroprotective Effect of Valproic Acid on Salicylate-Induced Tinnitus.International journal of molecular sciences · 2021
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Semax corrects brain dysfunction caused by prenatal introduction of valproic acid.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2013
    Article
  13. Article
  14. Chronic treatment with lithium or valproate modulates the expression of Homer1b/c and its related genes Shank and Inositol 1,4,5-trisphosphate receptor.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2012
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

5 authors at 3 institutions in 1 country.

Mireille BasselinBrain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg 9, Room 1S126, MSC 0947, 9 Memorial Drive, Bethesda, MD, 20892, USA. mirvasln@mail.nih.gov
Lisa Chang
Mei Chen
Jane M Bell
Stanley I Rapoport
Institute on Aging · USNational Institutes of Health · USNational Institute on Aging · 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
THE NERVOUS SYSTEM IN RELATION TO FUNCTION, AGING, AND DISEASEZ01AG000134 · NIA · NATIONAL INSTITUTE ON AGING · PI RAPOPORT, STANLEY I. · 1985 to 2008
$1.2M
Intramural NIH HHS Z01 AG000134
6 · The paper itself

Abstract

Evidence that brain glutamatergic activity is pathologically elevated in bipolar disorder suggests that mood stabilizers are therapeutic in the disease in part by downregulating glutamatergic activity. Such activity can involve the second messenger, arachidonic acid (AA, 20:4n - 6). We tested this hypothesis with regard to valproic acid (VPA), when stimulating glutamatergic N-methyl-D: -aspartate (NMDA) receptors in rat brain and measuring AA and related responses. An acute subconvulsant dose of NMDA (25 mg/kg i.p.) or saline was administered to unanesthetized rats that had been treated i.p. daily with VPA (200 mg/kg) or vehicle for 30 days. Quantitative autoradiography following intravenous [1-(14)C]AA infusion was used to image regional brain AA incorporation coefficients k*, markers of AA signaling. In chronic vehicle-pretreated rats, NMDA compared with saline significantly increased k* in 41 of 82 examined brain regions, many of which have high NMDA receptor densities, and also increased brain concentrations of the AA metabolites, prostaglandin E(2) (PGE(2)) and thromboxane B(2) (TXB(2)). VPA pretreatment reduced baseline concentrations of PGE(2) and TXB(2), and blocked the NMDA induced increases in k* and in eicosanoid concentrations. These results, taken with evidence that carbamazepine and lithium also block k* responses to NMDA in rat brain, suggest that mood stabilizers act in bipolar disorder in part by downregulating glutamatergic signaling involving AA.

Indexed as

AnimalsArachidonic AcidAutoradiographyBehavior, AnimalBrainDinoprostoneMaleN-MethylaspartateRatsRats, Inbred F344Signal TransductionThromboxane B2Valproic AcidArachidonic AcidDinoprostoneN-MethylaspartateThromboxane B2Valproic Acid

Identifiers

PMID18461450
PMCPMC2564799
OpenAlexW2040418863

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.