Evidence map›Paper›PMID 1322969›Full record

ArticleJournal of neurochemistry1992

Evidence for the implication of phosphoinositol signal transduction in mu-opioid inhibition of DNA synthesis.

J Barg, M M Belcheva, C J Coscia

Open access · greenAbstract read
In one paragraph

Article in Journal of neurochemistry, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 60 citations in OpenAlex.

  1. Morphine and gp120 toxic interactions in striatal neurons are dependent on HIV-1 strain.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012
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  4. Review
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  6. Adenosine receptor subtypes modulate two major functional pathways for hippocampal serotonin release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
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  15. Article
  16. Opioids inhibit endothelin-mediated DNA synthesis, phosphoinositide turnover, and Ca2+ mobilization in rat C6 glioma cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1994
    Article
  17. mu opiate receptor: cDNA cloning and expression.Proceedings of the National Academy of Sciences of the United States of America · 1993
    Article
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

J BargE. A. Doisy Department of Biochemistry and Molecular Biology, St. Louis University School of Medicine, Missouri 63104-1079.
M M Belcheva
C J Coscia
Saint Louis University · US

Funding

OPIOID MODULATION OF ASTROCYTE PROLIFERATIONR01DA005412 · NIDA · SAINT LOUIS UNIVERSITY · PI COSCIA, CARMINE JAMES · 1987 to 2008
$2.3M
NIDA NIH HHS DA 05412NIDA NIH HHS R01 DA005412
6 · The paper itself

Abstract

An opioid receptor agonist, [D-Ala2,Me-Phe4,Glyol5]enkephalin (DAMGE), decreased [3H]thymidine incorporation into DNA of fetal rat brain cell aggregates. This action proved to depend on the dose of this enkephalin analog and the interval the aggregates were maintained in culture. The opioid antagonist naltrexone and the mu-specific antagonist cyclic D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr amide (CTOP) reversed the DAMGE effect, arguing for a receptor-mediated mechanism. The mu-opioid nature of this receptor was further established by inhibiting DNA synthesis with the highly mu-selective agonist morphiceptin and blocking its action with CTOP. Several other opioids, pertussis toxin, and LiCl also diminished DNA synthesis, whereas cholera toxin elicited a modest increase. Naltrexone completely reversed the inhibition elicited by the combination of DAMGE and low doses of LiCl but not by that of high levels of LiCl alone. The enkephalin analog also reduced basal [3H]inositol trisphosphate and glutamate-stimulated [3H]inositol monophosphate and [3H]inositol bisphosphate accumulation in the aggregates. These DAMGE effects were reversed by naltrexone and were temporally correlated with the inhibition of DNA synthesis. A selective protein kinase C inhibitor, chelerythrine, also inhibited thymidine incorporation dose-dependently. The effect of DAMGE was not additive in the presence of chelerythrine but appeared to be consistent with their actions being mediated via a common signaling pathway. These results suggest the involvement of the phosphoinositol signal transduction system in the modulation of thymidine incorporation into DNA by DAMGE.

Indexed as

AnimalsCells, CulturedChloridesCholera ToxinDNAEnkephalin, Ala(2)-MePhe(4)-Gly(5)-EnkephalinsGTP-Binding ProteinsInositol PhosphatesLithiumLithium ChloridePertussis ToxinProtein Kinase CReceptors, OpioidReceptors, Opioid, muSignal TransductionChloridesCholera ToxinDNAEnkephalin, Ala(2)-MePhe(4)-Gly(5)-EnkephalinsGTP-Binding ProteinsInositol PhosphatesLithiumLithium ChloridePertussis ToxinProtein Kinase CReceptors, OpioidReceptors, Opioid, muThymidineVirulence Factors, Bordetella

Identifiers

PMID1322969
PMCPMC2571949
OpenAlexW2093521999

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.