Evidence map›Paper›PMID 22704858›Full record

ArticleExperimental neurology2012

Repetitive acute intermittent hypoxia increases expression of proteins associated with plasticity in the phrenic motor nucleus.

Irawan Satriotomo, Erica A Dale, Jenny M Dahlberg, Gordon S Mitchell

Abstract read
In one paragraph

Article in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 71 citations in OpenAlex.

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  7. Dose-dependent phosphorylation of endogenous Tau by intermittent hypoxia in rat brain.Journal of applied physiology (Bethesda, Md. : 1985) · 2022
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  15. Cervical spinal 5-HTJournal of applied physiology (Bethesda, Md. : 1985) · 2019
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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

4 authors at 1 institution in 1 country.

Irawan SatriotomoDepartment of Comparative Biosciences, University of Wisconsin, Madison, WI 53706, USA.
Erica A Dale
Jenny M Dahlberg
Gordon S Mitchell
University of Wisconsin–Madison · US

Funding

Stem Cell Therapy and Growth Factor Therapy for ALSP01NS057778 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI SVENDSEN, CLIVE NIELS · 2007 to 2011
$5.4M
Respiratory plasticity and spinal cord InjuryR37HL069064 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MITCHELL, GORDON S. · 2002 to 2011
$4.2M
Respiratory NeurobiologyT32HL007654 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MITCHELL, GORDON S. · 1987 to 2011
$4.0M
Mechanisms of respiratory long-term facilitationR01HL080209 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MITCHELL, GORDON S. · 2005 to 2013
$2.9M
Respiratory Plasticity and Spinal Cord InjuryR01HL069064 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MITCHELL, GORDON S. · 2014 to 2017
$1.5M
NHLBI NIH HHS HL007654NHLBI NIH HHS HL080209NHLBI NIH HHS HL69064NHLBI NIH HHS R01 HL069064NHLBI NIH HHS R01 HL080209NHLBI NIH HHS R37 HL069064NHLBI NIH HHS T32 HL007654NINDS NIH HHS NS057778NINDS NIH HHS P01 NS057778
6 · The paper itself

Abstract

Acute intermittent hypoxia (AIH) initiates plasticity in respiratory motor control, including phrenic long term facilitation (pLTF). Since pLTF is enhanced by preconditioning with repetitive exposure to AIH (rAIH), we hypothesized that a rAIH protocol consisting of 3 AIH exposures per week for 10 weeks (3×wAIH; AIH: 10, 5-min episodes of 10.5% O(2); 5-min normoxic intervals) would enhance expression of molecules that play key roles in pLTF within the phrenic motor nucleus. Immunohistochemical analyses revealed that 3×wAIH for 10 weeks increased serotonin terminal density in the C4 phrenic motor nucleus and serotonin 2A (5-HT(2A)) receptor expression in presumptive phrenic motor neurons. Immunoreactive brain derived neurotrophic factor (BDNF) and its high affinity receptor (TrkB) also increased following 3×wAIH. 3×wAIH also increased expression of another hypoxia-sensitive growth factor known to elicit phrenic motor facilitation, vascular endothelial growth factor (VEGF), and its receptor (VEGFR-2). Kinases "downstream" from TrkB and VEGFR-2 were up-regulated in or near presumptive phrenic motor neurons, including phosphorylated extracellular-signal regulated kinase (p-ERK) and protein kinase B (p-AKT). Thus, 3×wAIH up-regulates neurochemicals known to be associated with phrenic motor plasticity. Since 3×wAIH upregulates pro-plasticity molecules without evidence for CNS pathology, it may be a useful therapeutic tool in treating disorders that cause respiratory insufficiency, such as spinal injury or motor neuron disease.

Indexed as

Acute DiseaseAnimalsApoptosisGliosisHypoxiaMaleNerve Tissue ProteinsNeuronal PlasticityPhrenic NerveRandom AllocationRatsRats, Sprague-DawleyTime FactorsUp-RegulationNerve Tissue Proteins

Identifiers

PMID22704858
PMCPMC4375014
OpenAlexW2060230744

What OpenQuestion holds

Textmetadata
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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.