Evidence map›Paper›PMID 23638679›Full record

ArticleBritish journal of pharmacology2013

Functional interaction between pre-synaptic α6β2-containing nicotinic and adenosine A2A receptors in the control of dopamine release in the rat striatum.

P Garção, E C Szabó, S Wopereis, A A Castro, Â R Tomé, R D Prediger, R A Cunha, P Agostinho, A Köfalvi

Abstract read
In one paragraph

Article in British journal of pharmacology, 2013. 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
–field-weighted citation impact
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.

  1. Short-term nicotine deprivation alters dorsal anterior cingulate glutamate concentration and concomitant cingulate-cortical functional connectivity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Adenosine AInternational journal of molecular sciences · 2024
    Article
  9. Adenosine ABiomolecules · 2023
    Article
  10. Article
  11. Association Between Adenosine AMolecular neurobiology · 2021
    Article
  12. Review
  13. Article
  14. Review
  15. Crosstalk Between ATP-PFrontiers in cellular neuroscience · 2021
    Article
  16. Review
  17. Effects of an adenosine AJournal of psychopharmacology (Oxford, England) · 2020
    Article
  18. Novel Players in the Aging Synapse: Impact on Cognition.Journal of caffeine and adenosine research · 2019
    Review
  19. Article
  20. Review
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

9 authors.

P GarçãoCenter for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal; Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
E C Szabó
S Wopereis
A A Castro
 R Tomé
R D Prediger
R A Cunha
P Agostinho
A Köfalvi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposePre-synaptic nicotinic ACh receptors (nAChRs) and adenosine A2A receptors (A2A Rs) are involved in the control of dopamine release and are putative therapeutic targets in Parkinson's disease and addiction. Since A2A Rs have been reported to interact with nAChRs, here we aimed at mapping the possible functional interaction between A2A Rs and nAChRs in rat striatal dopaminergic terminals. EXPERIMENTAL APPROACH: We pharmacologically characterized the release of dopamine and defined the localization of nAChR subunits in rat striatal nerve terminals in vitro and carried out locomotor behavioural sensitization in rats in vivo. KEY

resultsIn striatal nerve terminals, the selective A2A R agonist CGS21680 inhibited, while the A2A R antagonist ZM241385 potentiated the nicotine-stimulated [(3) H]dopamine ([(3) H]DA) release. Upon blockade of the α6 subunit-containing nAChRs, the remaining nicotine-stimulated [(3) H]DA release was no longer modulated by A2A R ligands. In the locomotor sensitization experiments, nicotine enhanced the locomotor activity on day 7 of repeated nicotine injection, an effect that no longer persisted after 1 week of drug withdrawal. Notably, ZM241385-injected rats developed locomotor sensitization to nicotine already on day 2, which remained persistent upon nicotine withdrawal. CONCLUSIONS AND IMPLICATIONS: These results provide the first evidence for a functional interaction between nicotinic and adenosine A2A R in striatal dopaminergic terminals, with likely therapeutic consequences for smoking, Parkinson's disease and other dopaminergic disorders.

Indexed as

AdenosineAdenosine A2 Receptor AgonistsAdenosine A2 Receptor AntagonistsAnimalsCorpus StriatumDopamineGene Expression RegulationMaleMotor SkillsNicotinePhenethylaminesPresynaptic TerminalsRatsRats, WistarReceptor, Adenosine A2AReceptors, Nicotinic2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosineAdenosineAdenosine A2 Receptor AgonistsAdenosine A2 Receptor Antagonistsalpha6beta2 nicotinic acetylcholine receptorDopamineNicotinePhenethylaminesReceptor, Adenosine A2AReceptors, NicotinicTriazinesTriazolesZM 241385adenosineadenosine A2A receptoradenosine A2B receptordopaminelocomotor sensitizationnAChRsnicotineratstriatum

Identifiers

PMID23638679
PMCPMC3724115

What OpenQuestion holds

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Registered trials

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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.