Evidence map›Paper›PMID 23815362›Full record

ArticleJournal of neurochemistry2013

Growth hormone releasing hormone (GHRH) signaling modulates intermittent hypoxia-induced oxidative stress and cognitive deficits in mouse.

Deepti Nair, Vijay Ramesh, Richard C Li, Andrew V Schally, David Gozal

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

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  4. GHRH and its analogues in central nervous system diseases.Reviews in endocrine & metabolic disorders · 2025
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  16. Intermittent hypoxia suppression of growth hormone and insulin-like growth factor-I in the neonatal rat liver.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2018
    Article
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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

5 authors at 2 institutions in 1 country.

Deepti NairDepartment of Pediatrics, Pritzker School of Medicine, University of Chicago, Chicago, Illinois, USA.
Vijay Ramesh
Richard C Li
Andrew V Schally
David Gozal
University of Chicago · USSouth Florida Veterans Affairs Foundation for Research and Education · US

Funding

Oxidative stress in a murine model of sleep apneaR01HL086662 · NHLBI · UNIVERSITY OF LOUISVILLE · PI GOZAL, DAVID · 2008 to 2012
$1.9M
NHLBI NIH HHS HL-086662NHLBI NIH HHS R01 HL086662
6 · The paper itself

Abstract

Intermittent hypoxia (IH) during sleep, such as occurs in obstructive sleep apnea (OSA), leads to degenerative changes in the hippocampus, and is associated with spatial learning deficits in adult mice. In both patients and murine models of OSA, the disease is associated with suppression of growth hormone (GH) secretion, which is actively involved in the growth, development, and function of the central nervous system (CNS). Recent work showed that exogenous GH therapy attenuated neurocognitive deficits elicited by IH during sleep in rats. Here, we show that administration of the Growth Hormone Releasing Hormone (GHRH) agonist JI-34 attenuates IH-induced neurocognitive deficits, anxiety, and depression in mice along with reduction in oxidative stress markers such as MDA and 8-hydroxydeoxyguanosine, and increases in hypoxia inducible factor-1α DNA binding and up-regulation of insulin growth factor-1 and erythropoietin expression. In contrast, treatment with a GHRH antagonist (MIA-602) during intermittent hypoxia did not affect any of the IH-induced deleterious effects in mice. Thus, exogenous GHRH administered as the formulation of a GHRH agonist may provide a viable therapeutic intervention to protect IH-vulnerable brain regions from OSA-associated neurocognitive dysfunction. Sleep apnea, characterized by chronic intermittent hypoxia (IH), is associated with substantial cognitive and behavioral deficits. Here, we show that administration of a GHRH agonist (JI-34) reduces oxidative stress, increases both HIF-1α nuclear binding and downstream expression of IGF1 and erythropoietin (EPO) in hippocampus and cortex, and markedly attenuates water maze performance deficits in mice exposed to intermittent hypoxia during sleep.

Indexed as

Oxidative Stress8-Hydroxy-2'-DeoxyguanosineAnimalsCognition DisordersDeoxyguanosineDepressionErythropoietinGrowth Hormone-Releasing HormoneHypoxiaHypoxia-Inducible Factor 1, alpha SubunitLearning DisabilitiesLipid PeroxidationMaleMaze LearningMiceMice, Inbred C57BL8-Hydroxy-2'-DeoxyguanosineDeoxyguanosineErythropoietinGHRH(1-29)NH2, (PhAc-Ada)(0)-Tyr(1), Arg(2), Fpa(5,6), Ala(8), Har(9), Tyr(Me)(10), His(11), Orn(12,) Abu(15), His(20), Orn(21), Nle(27), Arg(28), Har(29)-Growth Hormone-Releasing HormoneHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitReceptor, IGF Type 1Sermorelin8-hydroxydeoxyguanosinecortexhippocampusintermittent hypoxiamalondialdehydeMorris water maze

Identifiers

PMID23815362
PMCPMC3851434
OpenAlexW1991037941

What OpenQuestion holds

Textmetadata
LicenceTDM
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.