Evidence map›Paper›PMID 27872762›Full record

ReviewNeural plasticity2016

Understanding the Functional Plasticity in Neural Networks of the Basal Ganglia in Cocaine Use Disorder: A Role for Allosteric Receptor-Receptor Interactions in A2A-D2 Heteroreceptor Complexes.

Dasiel O Borroto-Escuela, Karolina Wydra, Julia Pintsuk, Manuel Narvaez, Fidel Corrales, Magdalena Zaniewska, Luigi F Agnati, Rafael Franco, Sergio Tanganelli, Luca Ferraro and 2 more

Open access · goldAbstract readReview
In one paragraph

Review in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Allosteric Interactions between Adenosine AInternational journal of molecular sciences · 2021
    Review
  6. Adenosine ACells · 2020
    Review
  7. Article
  8. Article
  9. Dopamine DThe Journal of pharmacology and experimental therapeutics · 2018
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. 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

12 authors at 7 institutions in 6 countries.

Dasiel O Borroto-EscuelaDepartment of Neuroscience, Karolinska Institutet, Retzius väg 8. 17177 Stockholm, Sweden; Department of Biomolecular Science, Section of Physiology, University of Urbino, Campus Scientifico Enrico Mattei, Via Ca' le Suore 2, I-61029 Urbino, Italy; Observatorio Cubanos de Neurociencias, Grupo Bohío-Estudio, Yaguajay, Cuba.
Karolina WydraLaboratory of Drug Addiction Pharmacology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, PL-31-343 Kraków, Poland.
Julia PintsukDepartment of Neuroscience, Karolinska Institutet, Retzius väg 8. 17177 Stockholm, Sweden; Institute of Biomedicine and Translational Medicine, Department of Physiology, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia.
Manuel NarvaezUniversidad de Málaga, Instituto de Investigación Biomédica de Málaga, Facultad de Medicina, Málaga, Spain.
Fidel CorralesObservatorio Cubanos de Neurociencias, Grupo Bohío-Estudio, Yaguajay, Cuba; Universidad de Málaga, Instituto de Investigación Biomédica de Málaga, Facultad de Medicina, Málaga, Spain; Centro Nacional de Neurociencias, La Habana, Cuba.
Magdalena ZaniewskaLaboratory of Drug Addiction Pharmacology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, PL-31-343 Kraków, Poland.
Luigi F AgnatiDepartment of Neuroscience, Karolinska Institutet, Retzius väg 8. 17177 Stockholm, Sweden.
Rafael FrancoDepartament de Bioquímica i Biomedicina Molecular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain; Centro de Investigaciones en Red, Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain.
Sergio TanganelliDepartment of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy; Department of Medical Sciences, University of Ferrara, Ferrara, Italy.
Luca FerraroDepartment of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy.ORCID 0000-0003-2390-6414
Malgorzata FilipLaboratory of Drug Addiction Pharmacology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, PL-31-343 Kraków, Poland.
Kjell FuxeDepartment of Neuroscience, Karolinska Institutet, Retzius väg 8. 17177 Stockholm, Sweden.ORCID 0000-0001-8491-4288
Karolinska Institutet · SEMaj Institute of Pharmacology · PLUniversity of Ferrara · ITBiomedical Research Networking Center on Neurodegenerative Diseases · ESCuban Neuroscience Center · CUInstituto de Investigación Biomédica de Málaga · ESUniversity of Urbino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our hypothesis is that allosteric receptor-receptor interactions in homo- and heteroreceptor complexes may form the molecular basis of learning and memory. This principle is illustrated by showing how cocaine abuse can alter the adenosine A2AR-dopamine D2R heterocomplexes and their receptor-receptor interactions and hereby induce neural plasticity in the basal ganglia. Studies with A2AR ligands using cocaine self-administration procedures indicate that antagonistic allosteric A2AR-D2R heterocomplexes of the ventral striatopallidal GABA antireward pathway play a significant role in reducing cocaine induced reward, motivation, and cocaine seeking. Anticocaine actions of A2AR agonists can also be produced at A2AR homocomplexes in these antireward neurons, actions in which are independent of D2R signaling. At the A2AR-D2R heterocomplex, they are dependent on the strength of the antagonistic allosteric A2AR-D2R interaction and the number of A2AR-D2R and A2AR-D2R-sigma1R heterocomplexes present in the ventral striatopallidal GABA neurons. It involves a differential cocaine-induced increase in sigma1Rs in the ventral versus the dorsal striatum. In contrast, the allosteric brake on the D2R protomer signaling in the A2AR-D2R heterocomplex of the dorsal striatopallidal GABA neurons is lost upon cocaine self-administration. This is potentially due to differences in composition and allosteric plasticity of these complexes versus those in the ventral striatopallidal neurons.

Indexed as

Allosteric RegulationAnimalsBasal GangliaCocaineCocaine-Related DisordersHumansNerve NetNeuronal PlasticityPurinergic P1 Receptor AgonistsReceptor, Adenosine A2AReceptors, Dopamine D2Self AdministrationCocainePurinergic P1 Receptor AgonistsReceptor, Adenosine A2AReceptors, Dopamine D2

Identifiers

PMID27872762
PMCPMC5107220
OpenAlexW2546187623

What OpenQuestion holds

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LicenceCC BY
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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.