Evidence map›Paper›PMID 11027242›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

A common signaling pathway for striatal NMDA and adenosine A2a receptors: implications for the treatment of Parkinson's disease.

J E Nash, J M Brotchie

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

22 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Striatal GαFrontiers in cellular neuroscience · 2017
    Article
  8. Dopamine-Induced Changes in GαFrontiers in cellular neuroscience · 2017
    Article
  9. Review
  10. Review
  11. Therapy for Parkinson's disease: what is in the pipeline?Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2014
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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 2 institutions in 1 country.

J E NashManchester Movement Disorder Laboratory, Division of Neuroscience, School of Biological Sciences, University of Manchester, M13 9PT, United Kingdom.
J M Brotchie
Motac Neuroscience (United Kingdom) · GBUniversity of Manchester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The striatum is the major input region of the basal ganglia, playing a pivotal role in the selection, initiation, and coordination of movement both physiologically and in pathophysiological situations such as Parkinson's disease. In the present study, we characterize interactions between NMDA receptors, adenosine receptors, and cAMP signaling within the striatum. Both NMDA (100 micrometer) and the adenosine A(2a) receptor agonist CPCA (3 micrometer) increased cAMP levels (218.9 +/- 19.9% and 395.7 +/- 67.2%, respectively; cf. basal). The NMDA-induced increase in cAMP was completely blocked when slices were preincubated with either the NMDA receptor antagonist 7-chlorokynurenate or the adenosine A(2) receptor antagonist DMPX (100 micrometer), suggesting that striatal NMDA receptors increase cAMP indirectly via stimulation of adenosine A(2a) receptors. Thus, NMDA receptors and adenosine A(2a) receptors might share a common signaling pathway within the striatum. In striatal slices prepared from the 6-hydroxydopamine-lesioned rat model of Parkinson's disease, NMDA receptor-mediated increases in cAMP were greater on the lesioned side compared with the unlesioned side (349.6 +/- 40.2% compared with 200.9 +/- 21.9% of basal levels, respectively). This finding substantiates previous evidence implicating overactivity of striatal NMDA receptors in parkinsonism and suggests that a common NMDA receptor-adenosine A(2a) receptor-cAMP signaling cascade might be an important mechanism responsible for mediating parkinsonian symptoms.

Indexed as

3,4-Dihydroxyphenylacetic AcidAnalysis of VarianceAnimalsCorpus StriatumCyclic AMPDisease Models, AnimalDopamineDose-Response Relationship, DrugExcitatory Amino Acid AntagonistsIn Vitro TechniquesMaleNeuroprotective AgentsN-MethylaspartateOxidopamineParkinson Disease, SecondaryPurinergic P1 Receptor Agonists3,4-Dihydroxyphenylacetic AcidCyclic AMPDopamineExcitatory Amino Acid AntagonistsNeuroprotective AgentsN-MethylaspartateOxidopaminePurinergic P1 Receptor AgonistsPurinergic P1 Receptor AntagonistsReceptor, Adenosine A2AReceptors, N-Methyl-D-AspartateReceptors, Purinergic P1

Identifiers

PMID11027242
PMCPMC6772864
OpenAlexW1946075667

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.