Evidence map›Paper›PMID 10024356›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Activation of human D3 dopamine receptor inhibits P/Q-type calcium channels and secretory activity in AtT-20 cells.

E V Kuzhikandathil, G S Oxford

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Abnormalities of Dopamine DJournal of central nervous system disease · 2017
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Dopamine D3 receptor antagonism inhibits cocaine-seeking and cocaine-enhanced brain reward in rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  15. Amphetamine blocks long-term synaptic depression in the ventral tegmental area.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000
    Article
  16. 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

2 authors at 1 institution in 1 country.

E V KuzhikandathilDepartment of Cell and Molecular Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
G S Oxford
University of North Carolina at Chapel Hill · US

Funding

IONIC MECHANISMS RELATED TO SECRETION IN PITUITARY CELLSR01NS018788 · NINDS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI OXFORD, GERRY S · 1985 to 2002
$908k
NINDS NIH HHS NS18788NINDS NIH HHS R01 NS018788
6 · The paper itself

Abstract

The D3 dopamine receptor is postulated to play an important role in the regulation of neurotransmitter secretion at both pre- and postsynaptic terminals. However, this hypothesis and the underlying mechanisms remain untested because of the lack of D3-selective ligands, paucity of appropriate model secretory systems, and the weak and inconsistent coupling of D3 receptors to classical signal transduction pathways. The absence of ligands that selectively discriminate between D3 and D2 receptors in vivo precludes the study of D3 receptor function in the brain and necessitates the use of heterologous expression systems. In this report we demonstrate that activation of the human D3 dopamine receptor expressed in the AtT-20 neuroendocrine cell line causes robust inhibition of P/Q-type calcium channels via pertussis toxin-sensitive G-proteins. In addition, using the vesicle trafficking dye FM1-43, we show that D3 receptor activation significantly inhibits spontaneous secretory activity in these cells. Our results not only support the hypothesis that the D3 receptor can regulate secretory activity but also provide insight into the underlying signaling mechanisms. We propose a functional model in which the D3 receptor tightly regulates neurotransmitter release at a synapse by only allowing the propagation of spikes above a certain frequency or burst-duration threshold.

Indexed as

Calcium Channels, N-TypeGTP-Binding Protein alpha SubunitsHeterotrimeric GTP-Binding ProteinsAnimalsBariumCalciumCalcium Channel BlockersCalcium ChannelsCalcium Channels, L-TypeCell LineCytoplasmic GranulesDopamine AgonistsGTP-Binding Protein alpha Subunits, Gi-GoGTP-Binding ProteinsHumansIn Vitro TechniquesBariumCalciumCalcium Channel BlockersCalcium ChannelsCalcium Channels, L-TypeCalcium Channels, N-TypeDopamine AgonistsDRD3 protein, humanDrd3 protein, mouseGNAZ protein, humanGnaz protein, mouseGTP-Binding Protein alpha SubunitsGTP-Binding Protein alpha Subunits, Gi-GoGTP-Binding ProteinsHeterotrimeric GTP-Binding ProteinsNimodipinePertussis ToxinQuinpiroleReceptors, Dopamine D2Receptors, Dopamine D3SomatostatinVirulence Factors, Bordetella

Identifiers

PMID10024356
PMCPMC6782181
OpenAlexW2103299253

What OpenQuestion holds

Texttitle and abstract
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.