Evidence map›Paper›PMID 31455661›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019

Transient Hypoxemia Disrupts Anatomical and Functional Maturation of Preterm Fetal Ovine CA1 Pyramidal Neurons.

Evelyn McClendon, Kang Wang, Kiera Degener-O'Brien, Matthew W Hagen, Xi Gong, Thuan Nguyen, Wendy W Wu, James Maylie, Stephen A Back

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. 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
–field-weighted citation impact
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.

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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

9 authors.

Evelyn McClendonDepartment of Pediatrics.ORCID 0000-0003-3541-189X
Kang WangObstetrics and Gynecology, and.
Kiera Degener-O'BrienDepartment of Pediatrics.
Matthew W HagenDepartment of Pediatrics.ORCID 0000-0002-9812-2262
Xi GongDepartment of Pediatrics.
Thuan NguyenPublic Health and Preventive Medicine.
Wendy W WuObstetrics and Gynecology, and.
James MaylieObstetrics and Gynecology, and.
Stephen A BackDepartment of Pediatrics, backs@ohsu.edu.

Funding

Role of Extracellular Matrix in Hypoxic-Ischemic Perinatal White Matter InjuryR01NS054044 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2006 to 2021
$4.8M
Cellular Mechanisms of Fetal White Matter InjuryR01NS045737 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2003 to 2019
$3.7M
Cellular mechanisms of fetal white matter injuryR37NS045737 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2007 to 2013
$2.7M
NINDS NIH HHS R01 NS045737NINDS NIH HHS R01 NS054044NINDS NIH HHS R37 NS045737
6 · The paper itself

Abstract

Children who survive premature birth often exhibit reductions in hippocampal volumes and deficits in working memory. However, it is unclear whether synaptic plasticity and cellular mechanisms of learning and memory can be elicited or disrupted in the preterm fetal hippocampus. CA1 hippocampal neurons were exposed to two common insults to preterm brain: transient hypoxia-ischemia (HI) and hypoxia (Hx). We used a preterm fetal sheep model using both sexes in twin 0.65 gestation fetuses that reproduces the spectrum of injury and abnormal growth in preterm infants. Using Cavalieri measurements, hippocampal volumes were reduced in both Hx and HI fetuses compared with controls. This volume loss was not the result of neuronal cell death. Instead, morphometrics revealed alterations in both basal and apical dendritic arborization that were significantly associated with the level of systemic hypoxemia and metabolic stress regardless of etiology. Anatomical alterations of CA1 neurons were accompanied by reductions in probability of presynaptic glutamate release, long-term synaptic plasticity and intrinsic excitability. The reduction in intrinsic excitability was in part due to increased activity of the channels underlying the fast and slow component of the afterhyperpolarization in Hx and HI. Our studies suggest that even a single brief episode of hypoxemia can markedly disrupt hippocampal maturation. Hypoxemia may contribute to long-term working memory disturbances in preterm survivors by disrupting neuronal maturation with resultant functional disturbances in hippocampal action potential throughput. Strategies directed at limiting the duration or severity of hypoxemia during brain development may mitigate disturbances in hippocampal maturation.

Indexed as

AnimalsCA1 Region, HippocampalDendritesDendritic SpinesFemaleFetal DevelopmentHypoxiaMaleMemory, Long-TermMemory, Short-TermNeuronal PlasticityPregnancyPremature BirthPyramidal CellsSheepStress, Physiologicaldendritic morphologydevelopmental neuroanatomyelectrophysiologyhippocampusLTPsynaptic plasticity

Identifiers

PMID31455661
PMCPMC6774402

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.