Evidence map›Paper›PMID 10373698›Full record

ArticleThe Journal of physiology1999

Adenosinergic modulation of respiratory neurones in the neonatal rat brainstem in vitro.

E Herlenius, H Lagercrantz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

19 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Article
  6. Review
  7. Caffeine therapy in preterm infants.World journal of clinical pediatrics · 2015
    Review
  8. Article
  9. Article
  10. Article
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  13. Article
  14. Article
  15. Article
  16. P2Y1 receptor modulation of the pre-Bötzinger complex inspiratory rhythm generating network in vitro.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  17. Article
  18. Adenosine A1 receptors reduce release from excitatory but not inhibitory synaptic inputs onto lateral horn neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  19. Hyperalgesia, anxiety, and decreased hypoxic neuroprotection in mice lacking the adenosine A1 receptor.Proceedings of the National Academy of Sciences of the United States of America · 2001
    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 2 countries.

E HerleniusKarolinska Institutet, Neonatal Unit, Department of Woman and Child Health, Astrid Lindgren Children's Hospital, S-171 76 Stockholm, Sweden. eric.herlenius@dsg.ki.se
H Lagercrantz
Boston Children's Hospital · USKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The mechanism underlying adenosinergic modulation of respiration was examined in vitro by applying the whole-cell patch-clamp technique to different types of respiration-related neurones located in the rostral ventrolateral medulla of neonatal rats (0-4 days old). 2. The adenosine A1-receptor agonist (R)-N6-(2-phenylisopropyl)-adenosine (R-PIA, 10 microM; n = 31) increased the burst distance of rhythmic C4 inspiratory discharges and decreased the duration of inspiratory discharges (control: 8.00 +/- 2.49 s and 918 +/- 273 ms; R-PIA: 12.10 +/- 5.60 s and 726 +/- 215 ms). 3. Expiratory neurones demonstrated a reversible decrease in input resistance (Rin), a depression of action potential discharges and a hyperpolarization of the membrane potential (Vm) during application of R-PIA (1-10 microM). Similar responses of Rin and Vm to R-PIA were evident after synaptic activity had been blocked by 0.5 microM tetrodotoxin (TTX). 4. Some of the biphasic expiratory (biphasic E) neurones, but none of the inspiratory neurones, demonstrated changes in Rin or Vm during R-PIA application. With TTX present, R-PIA did not alter Vm or Rin in biphasic expiratory or inspiratory neurones. 5. Furthermore, R-PIA decreased the spontaneous postsynaptic activities of all neurones examined. The effects of R-PIA on respiratory activity, Rin and Vm could be reversed by the A1-receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX; 200 nM). 6. Our data suggest that the modulation of respiratory output induced by adenosinergic agents can be explained by (1) a general decrease in synaptic transmission between medullary respiration-related neurones mediated by presynaptic A1-receptors, and (2) an inactivation, via membrane hyperpolarization, of medullary expiratory neurones mediated by postsynaptic A1-receptors. Furthermore, our data demonstrate that inactivation of expiratory neurones does not abolish the respiratory rhythmic activity, but only modulates respiratory rhythm in vitro.

Indexed as

AdenosineAirway ResistanceAnimalsAnimals, NewbornBrain StemElectrophysiologyIn Vitro TechniquesMembrane PotentialsMotor NeuronsNeuronsPatch-Clamp TechniquesPurinergic P1 Receptor AntagonistsRatsRats, WistarReceptors, Purinergic P1Respiratory Mechanics1,3-dipropyl-8-cyclopentylxanthineAdenosinePurinergic P1 Receptor AntagonistsReceptors, Purinergic P1Xanthines

Identifiers

PMID10373698
PMCPMC2269420
OpenAlexW2085300954

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.