Evidence map›Paper›PMID 8350262›Full record

ArticleThe Journal of physiology1993

Modulation of respiratory activity of neonatal rat phrenic motoneurones by serotonin.

A D Lindsay, J L Feldman

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.9field-weighted citation impact, top 2% 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

56 citing papers in PubMed, 179 citations in OpenAlex.

  1. Trial
  2. Article
  3. Loss of 5-HTFrontiers in neural circuits · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. AAV2-BDNF promotes respiratory axon plasticity and recovery of diaphragm function following spinal cord injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  10. 5-HTThe Journal of physiology · 2019
    Article
  11. Review
  12. Breathing: Motor Control of Diaphragm Muscle.Physiology (Bethesda, Md.) · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

A D LindsayDepartment of Physiological Science, University of California Los Angeles 90024-1527.
J L Feldman
Department of Physiological Sciences · RU

Funding

TRANSMISSION OF RESPIRATORY DRIVE TO PHRENIC MOTONEURONSR01NS024742 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FELDMAN, JACK L · 1986 to 2008
$2.7M
MOTONEURON PROPERTIES STUDIED IN VITROF32NS008530 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LINDSAY, AMY D · 1988 to 1990
–
NINDS NIH HHS NS 08530NINDS NIH HHS NS24742
6 · The paper itself

Abstract

1. The effects of serotonin on phrenic motoneurones were studied in an in vitro preparation of the isolated brainstem and spinal cord from neonatal rats. 2. Serotonin (5-HT; > or = 5-10 microM) increased inspiratory-modulated phrenic nerve activity and produced a small amount of tonic activity during expiration. Inspiratory-modulated activity of the fourth cervical ventral root also increased, but was accompanied by robust tonic activity, which often obscured the rhythmic activity. 3. Serotonin, in both normal and tetrodotoxin-containing medium, depolarized phrenic motoneurones and increased cell input resistance. Serotonin also increased inspriatory-modulated firing as well as the response of phrenic motoneurones to injected current. The y-intercept of the relationship between firing frequency and injected current (f-I) was increased, but the slope was not affected. There was no bistable firing behaviour. 4. Under voltage clamp conditions, 5-HT produced a tonic inward current of 0.07-0.37 nA. This current increased with less negative holding potentials and decreased with more negative holding potentials (-75 to -90 mV) but did not reverse. 5. In addition, 5-HT decreased inspiratory-modulated synaptic current by 23 +/- 6%. The degree of attenuation was not affected by holding potential. The time course of the decrease in inspiratory-modulated synaptic current was similar to the changes seen in tonic inward current and input resistance. 6. Depolarization, tonic inward current, and shift in the f-I relationship produced by 5-HT were antagonized by the 5-HT2/1C receptor antagonist ketanserin and mimicked by the 5-HT2/1C agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). However, the 5-HT induced decrease in inspiratory-modulated synaptic current was not reduced by ketanserin nor mimicked by DOI. 7. We conclude that exogenously applied 5-HT simultaneously increases cell excitability and decreases inspiratory-modulated synaptic current in phrenic motoneurones via different types of receptors. When these responses occurred simultaneously, the increase in excitability predominated and the net effect was an augmentation of inspiratory-modulated phrenic motoneurone activity.

Indexed as

AnimalsCulture TechniquesElectrophysiologyMembrane PotentialsMotor NeuronsPhrenic NerveRatsRats, Sprague-DawleyRespirationSerotoninSerotonin

Identifiers

PMID8350262
PMCPMC1175254
OpenAlexW2050875515

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.