Evidence map›Paper›PMID 17446223›Full record

ArticleThe Journal of physiology2007

Control of basal extracellular adenosine concentration in rat cerebellum.

Mark J Wall, Alison Atterbury, Nicholas Dale

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 65 citations in OpenAlex.

  1. NADInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Effects of the ecto-ATPase apyrase on microglial ramification and surveillance reflect cell depolarization, not ATP depletion.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  7. Article
  8. Reducing Extracellular CaFrontiers in neural circuits · 2017
    Article
  9. Article
  10. Cell type-specific effects of adenosine on cortical neurons.Cerebral cortex (New York, N.Y. : 1991) · 2015
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cellular mechanisms and behavioral consequences of Kv1.2 regulation in the rat cerebellum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  18. Article
  19. Deletion of ecto-5'-nucleotidase (CD73) reveals direct action potential-dependent adenosine release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  20. Purinergic modulation of granule cells.Cerebellum (London, England) · 2012
    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

3 authors at 1 institution in 1 country.

Mark J WallNeuroscience Group, Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, UK. mark.wall@warwick.ac.uk
Alison Atterbury
Nicholas Dale
University of Warwick · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

To re-examine how the basal extracellular concentration of adenosine is regulated in acutely isolated cerebellar slices we have combined electrophysiological and microelectrode biosensor measurements. In almost all cases, synaptic transmission was tonically inhibited by adenosine acting via A1 receptors. By contrast, in most slices, the biosensors did not measure an adenosine tone but did record a spatially non-uniform extracellular tone of the downstream metabolites (inosine and hypoxanthine). Most of the extracellular hypoxanthine arose from the metabolism of inosine by ecto-purine nucleoside phosphorylase (PNP). Adenosine kinase was the major determinant of adenosine levels, as its inhibition increased both adenosine concentration and A1 receptor-mediated synaptic inhibition. Breakdown of adenosine by adenosine deaminase was the major source of the inosine/hypoxanthine tone. However adenosine deaminase played a minor role in determining the level of adenosine at synapses, suggesting a distal location. Blockade of adenosine transport (by NBTI/dipyridamole) had inconsistent effects on basal levels of adenosine and synaptic transmission. Unexpectedly, application of NBTI/dipyridamole prevented the efflux of adenosine resulting from block of adenosine kinase at only a subset of synapses. We conclude that there is spatial variation in the functional expression of NBTI/dipyridamole-sensitive transporters. The increased spatial and temporal resolution of the purine biosensor measurements has revealed the complexity of the control of adenosine and purine tone in the cerebellum.

Indexed as

Neural InhibitionSynaptic TransmissionAdenosineAdenosine DeaminaseAdenosine KinaseAdenosine TriphosphateAnimalsBiosensing TechniquesCerebellumElectric StimulationElectrophysiologyEquilibrative Nucleoside Transport ProteinsExcitatory Postsynaptic PotentialsExtracellular SpaceHypoxanthineInosineAdenosineAdenosine DeaminaseAdenosine KinaseAdenosine TriphosphateEquilibrative Nucleoside Transport ProteinsHypoxanthineInosineNucleobase Transport ProteinsPurine-Nucleoside PhosphorylaseReceptor, Adenosine A1

Identifiers

PMID17446223
PMCPMC2075308
OpenAlexW2157990225

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.