Evidence map›Paper›PMID 22422797›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2012

Effect of hyperoxic exposure during early development on neurotrophin expression in the carotid body and nucleus tractus solitarii.

Raul Chavez-Valdez, Ariel Mason, Ana R Nunes, Frances J Northington, Clarke Tankersley, Rajni Ahlawat, Sheree M Johnson, Estelle B Gauda

Abstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2012. 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
1.5field-weighted citation impact, top 20% 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, 28 citations in OpenAlex.

  1. Observational
  2. Article
  3. Article
  4. Neurochemical Plasticity of the Carotid Body.Advances in anatomy, embryology, and cell biology · 2023
    Article
  5. Article
  6. Article
  7. Growth Factors in the Carotid Body-An Update.International journal of molecular sciences · 2020
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Proposed toxic and hypoxic impairment of a brainstem locus in autism.International journal of environmental research and public health · 2013
    Article
  17. Review
  18. Review
  19. Chronic hyperoxia and the development of the carotid body.Respiratory physiology & neurobiology · 2013
    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

8 authors at 4 institutions in 2 countries.

Raul Chavez-ValdezDepartment of Pediatrics, Division of Neonatology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287-3200, USA.
Ariel Mason
Ana R Nunes
Frances J Northington
Clarke Tankersley
Rajni Ahlawat
Sheree M Johnson
Estelle B Gauda
Johns Hopkins University · USJohns Hopkins Medicine · USHoward University · USTexas Tech University · US

Funding

Neuroplasticity and the carotid bodyR01HL080725 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI GAUDA, ESTELLE B. · 2006 to 2009
$1.6M
CO2/H+ Modulation of Rhythmogenic Inspiratory NeuronsK01NS047422 · NINDS · HOWARD UNIVERSITY · PI JOHNSON, SHEREE M · 2004 to 2009
$718k
NHLBI NIH HHS R01HL080725NINDS NIH HHS 5K01NS047422
6 · The paper itself

Abstract

Synaptic activity can modify expression of neurotrophins, which influence the development of neuronal circuits. In the newborn rat, early hyperoxia silences the synaptic activity and input from the carotid body, impairing the development and function of chemoreceptors. The purpose of this study was to determine whether early hyperoxic exposure, sufficient to induce hypoplasia of the carotid body and decrease the number of chemoafferents, would also modify neurotrophin expression within the nucleus tractus solitarii (nTS). Rat pups were exposed to hyperoxia (fraction of inspired oxygen 0.60) or normoxia until 7 or 14 days of postnatal development (PND). In the carotid body, hyperoxia decreased brain-derived neurotrophic factor (BDNF) protein expression by 93% (P = 0.04) after a 7-day exposure, followed by a decrease in retrogradely labeled chemoafferents by 55% (P = 0.004) within the petrosal ganglion at 14 days. Return to normoxia for 1 wk after a 14-day hyperoxic exposure did not reverse this effect. In the nTS, hyperoxia for 7 days: 1) decreased BDNF gene expression by 67% and protein expression by 18%; 2) attenuated upregulation of BDNF mRNA levels in response to acute hypoxia; and 3) upregulated p75 neurotrophic receptor, truncated tropomyosin kinase B (inactive receptor), and cleaved caspase-3. These effects were not observed in the locus coeruleus (LC). Hyperoxia for 14 days also decreased tyrosine hydroxylase levels by 18% (P = 0.04) in nTS but not in the LC. In conclusion, hyperoxic exposure during early PND reduces neurotrophin levels in the carotid body and the nTS and shifts the balance of neurotrophic support from prosurvival to proapoptotic in the nTS, the primary brain stem site for central integration of sensory and autonomic inputs.

Indexed as

Age FactorsAnimalsAnimals, NewbornApoptosisBrain-Derived Neurotrophic FactorCarotid BodyCaspase 3Cell SurvivalDisease Models, AnimalHyperoxiaNerve Tissue ProteinsProtein KinasesRatsRats, Sprague-DawleyReceptors, Growth FactorReceptors, Nerve Growth FactorBrain-Derived Neurotrophic FactorCasp3 protein, ratCaspase 3Nerve Tissue ProteinsNgfr protein, ratProtein KinasesReceptors, Growth FactorReceptors, Nerve Growth FactorRNA, Messengertropomyosin kinaseTyrosine 3-Monooxygenase

Identifiers

PMID22422797
PMCPMC3365411
OpenAlexW2088720479

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.