Evidence map›Paper›PMID 18096663›Full record

ArticleEndocrinology2008

Dopamine inhibits basal prolactin release in pituitary lactotrophs through pertussis toxin-sensitive and -insensitive signaling pathways.

Arturo E Gonzalez-Iglesias, Takayo Murano, Shuo Li, Melanija Tomić, Stanko S Stojilkovic

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 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
0.8field-weighted citation impact, top 29% 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, 44 citations in OpenAlex.

  1. Review
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  8. Review
  9. Review
  10. Review of serum prolactin levels as an antipsychotic-response biomarker.Open access journal of translational medicine & research · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. cAMP-mediated stabilization of fusion pores in cultured rat pituitary lactotrophs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  16. Article
  17. Article
  18. Review
  19. Article
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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 2 institutions in 1 country.

Arturo E Gonzalez-IglesiasNational Institute of Child Health and Human Development, 49 Convent Drive, Bethesda, MD 20892-4510, USA.
Takayo Murano
Shuo Li
Melanija Tomić
Stanko S Stojilkovic
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Institutes of Health · US

Funding

Intracellular Signaling In Endocrine CellsZIAHD000195 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI STOJILKOVIC, STANKO S. · 2009 to 2025
$18.8M
INTRACELLULAR SIGNALING IN ENDOCRINE CELLSZ01HD000195 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI STOJILKOVIC, STANKO S. · 1994 to 2008
$2.4M
Intramural NIH HHS
6 · The paper itself

Abstract

Dopamine D2 receptors signal through the pertussis toxin (PTX)-sensitive G(i/o) and PTX-insensitive G(z) proteins, as well as through a G protein-independent, beta-arrestin/glycogen synthase kinase-3-dependent pathway. Activation of these receptors in pituitary lactotrophs leads to inhibition of prolactin (PRL) release. It has been suggested that this inhibition occurs through the G(i/o)-alpha protein-mediated inhibition of cAMP production and/or G(i/o)-betagamma dimer-mediated activation of inward rectifier K(+) channels and inhibition of voltage-gated Ca(2+) channels. Here we show that the dopamine agonist-induced inhibition of spontaneous Ca(2+) influx and release of prestored PRL was preserved when cAMP levels were elevated by forskolin treatment. We further observed that dopamine agonists inhibited both spontaneous and depolarization-induced Ca(2+) influx in untreated but not in PTX-treated cells. This inhibition was also observed in cells with blocked inward rectifier K(+) channels, suggesting that the dopamine effect on voltage-gated Ca(2+) channel gating is sufficient to inhibit spontaneous Ca(2+) influx. However, agonist-induced inhibition of PRL release was only partially relieved in PTX-treated cells, indicating that dopamine receptors also inhibit exocytosis downstream of voltage-gated Ca(2+) influx. The PTX-insensitive step in agonist-induced inhibition of PRL release was not affected by the addition of wortmannin, an inhibitor of phosphatidylinositol 3-kinase, and lithium, an inhibitor of glycogen synthase kinase-3, but was attenuated in the presence of phorbol 12-myristate 13-acetate, which inhibits G(z) signaling pathway in a protein kinase C-dependent manner. Thus, dopamine inhibits basal PRL release by blocking voltage-gated Ca(2+) influx through the PTX-sensitive signaling pathway and by desensitizing Ca(2+) secretion coupling through the PTX-insensitive and protein kinase C-sensitive signaling pathway.

Indexed as

Adenylyl Cyclase InhibitorsAndrostadienesAnimalsCalciumCells, CulturedCyclic AMPDopamineFemaleLithiumPertussis ToxinPituitary GlandPotassium Channels, Inwardly RectifyingProlactinRatsRats, Sprague-DawleySignal TransductionAdenylyl Cyclase InhibitorsAndrostadienesCalciumCyclic AMPDopamineLithiumPertussis ToxinPotassium Channels, Inwardly RectifyingProlactinTetradecanoylphorbol AcetateWortmannin

Identifiers

PMID18096663
PMCPMC2276716
OpenAlexW2038660215

What Socratic 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 Socratic graph.