Evidence map›Paper›PMID 12574410›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

D5 (not D1) dopamine receptors potentiate burst-firing in neurons of the subthalamic nucleus by modulating an L-type calcium conductance.

Jérôme Baufreton, Maurice Garret, Alicia Rivera, Adélaïda de la Calle, François Gonon, Bernard Dufy, Bernard Bioulac, Anne Taupignon

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

39 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
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  3. Dopamine internalization via UptakeFrontiers in pharmacology · 2024
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  13. Group I mGluRs evoke K-ATP current by intracellular Ca2+ mobilization in rat subthalamus neurons.The Journal of pharmacology and experimental therapeutics · 2013
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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

8 authors at 1 institution in 1 country.

Jérôme BaufretonSignalisation Normale et Pathologique, Unité Mixte de Recherche 5543, Université Victor Segalen, 33076 Bordeaux Cedex, France.
Maurice Garret
Alicia Rivera
Adélaïda de la Calle
François Gonon
Bernard Dufy
Bernard Bioulac
Anne Taupignon
Universidad de Málaga · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dopamine is a crucial factor in basal ganglia functioning. In current models of basal ganglia, dopamine is postulated to act on striatal neurons. However, it may also act on the subthalamic nucleus (STN), a key nucleus in the basal ganglia circuit. The data presented here were obtained in brain slices using whole-cell patch clamp. They reveal that D5 dopamine receptors strengthen electrical activity in the subset of subthalamic neurons endowed with burst-firing capacity, resulting in longer discharges of spontaneous or evoked bursts. To distinguish between D1 and D5 subtypes, the action of agonists in the D1/D5 receptor family was first investigated on rat subthalamic neurons. Single-cell reverse transcription-PCR profiling showed that burst-competent neurons only expressed D5 receptors. Accordingly, receptors localized in postsynaptic membranes within the STN were labeled by a D5-specific antibody. Second, agonists in the D1/D5 family were tested in mouse brain slices. It was found that these agonists were active in D1 receptor knock-out mice in a similar way to wild-type mice or rats. This proved that D5 rather than D1 receptors were involved. Pharmacological tools (dihydropyridines, omega-conotoxins, and calciseptine) were used to identify the target of D5 receptors as an L-type channel. This was reached via G-protein and protein kinase A. The action of dopamine on D5 receptors therefore shapes neuronal activity. It contributes to normal information processing in basal ganglia outside striatum. This finding may be useful in drug therapy for various disorders involving changes in STN activity, such as Parkinson's disease and related disorders.

Indexed as

AnimalsCalcium Channel BlockersCalcium Channels, L-TypeCyclic AMP-Dependent Protein KinasesDopamine AgonistsEnzyme InhibitorsExcitatory Amino Acid AgonistsGTP-Binding ProteinsIn Vitro TechniquesMembrane PotentialsMiceMice, KnockoutNeuronsPatch-Clamp TechniquesPotassium Channel BlockersRatsCalcium Channel BlockersCalcium Channels, L-TypeCyclic AMP-Dependent Protein KinasesDopamine AgonistsDrd5 protein, mouseDrd5 protein, ratEnzyme InhibitorsExcitatory Amino Acid AgonistsGTP-Binding ProteinsPotassium Channel BlockersReceptors, Dopamine D1Receptors, Dopamine D5

Identifiers

PMID12574410
PMCPMC6741933
OpenAlexW2096757255

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.