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Lack of oxygen, not blood flow, delays preemie brain

Research challenges more than a decade of scientific study and clinical understanding of brain development...

Lack of oxygen, and not blood flow, is what delays brain maturation in preterm infants New research from OHSU Doernbecher Children's Hospital in Portland, Oregon, rebuts decades of previous scientific understanding, suggests opportunity to restore, reduce life-long impacts of brain injury

Premature infants are at risk for a broad spectrum of life-long cognitive and learning disabilities. Historically, these conditions were believed to be the result of lack of blood flow to the brain. However, a new study published in the Journal of Neuroscience, finds that while limited blood flow may contribute, major disturbances are actually caused by low oxygen.

This research challenges more than a decade of scientific study and clinical understanding of brain development in preterm children, said the study's principal investigator Stephen Back, MD PhD, Clyde and Elda Munson Professor of Pediatric Research and Pediatrics, Oregon Health & Science University (OHSU) School of Medicine, OHSU Doernbecher.
"Previously, we thought lack of blood flow was causing preterm brain cells to die. Instead, these critically important cells simply fail to develop normally. This finding creates an opportunity to determine ways to restore oxygen loss and potentially reduce life-long impacts of preterm survivors."

Stephen Back MD PhD, Clyde and Elda Munson Professor of Pediatric Research and Pediatrics, Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA.

Using a preterm sheep model, Back and his team analyzed the response of fetal subplate neurons - the cells that play a critical role in regulating preterm brain function and connectivity - to disturbances of brain oxygenation. When the developing brain was exposed to lower than normal rates of oxygen for as short as 25 minutes, subplate neurons showed major long-term disturbances just one month following exposure.

"This brief exposure to low oxygen occurs frequently in preterm babies receiving care in a neonatal intensive care unit," said Back. "And this result better explains the long-term complications that these preterm babies sustain as they grow older, which include significant challenges with learning, memory and attention."

Although additional research is needed to determine the exact developmental timeframes for potential injury due to oxygen loss in infants, as well as the optimal concentration of oxygen needed for early intervention therapy, Back believes the findings suggest a need to re-evaluate current practices in intensive care settings.
"Given this new range of opportunity to promote brain repair, clinicians must critically rethink how to interact with, stimulate and handle preterm babies during intensive care treatment. This will help to better manage transient low-oxygen states and determine what the preterm brain can and cannot tolerate."

Stephen Back MD PhD.

Preterm infants are at risk for a broad spectrum of neurobehavioral disabilities associated with diffuse disturbances in cortical growth and development. During brain development, subplate neurons (SPNs) are a largely transient population that serves a critical role to establish functional cortical circuits. By dynamically integrating into developing cortical circuits they assist in consolidation of intra and extracortical circuits. Although SPNs reside in close proximity to cerebral white matter, which is particularly vulnerable to oxidative stress, the susceptibility of SPNs remains controversial. We determined SPN responses to two common insults to the preterm brain, hypoxia-ischemia and hypoxia. We employed a preterm fetal sheep model using both sexes that reproduces the spectrum of human cerebral injury and abnormal cortical growth. Unlike oligodendrocyte progenitors, SPNs displayed pronounced resistance to early or delayed cell death from hypoxia or hypoxia-ischemia. We thus explored an alternative hypothesis that these insults alter the maturational trajectory of SPNs. We employed DiOlistic labeling to visualize the dendrites of SPNs selectively labeled for complexin-3. SPNs displayed reduced basal dendritic arbor complexity that was accompanied by chronic disturbances in SPN excitability and synaptic activity. SPN dysmaturation was significantly associated with the level of fetal hypoxemia and metabolic stress. Hence, despite the resistance of SPNs to insults that trigger white matter injury, transient hypoxemia disrupted SPN arborization and functional maturation during a critical window in cortical development. Strategies directed at limiting the duration or severity of hypoxemia during brain development may mitigate disturbances in cerebral growth and maturation related to SPN dysmaturation.

Signifigance Statement
The human preterm brain commonly sustains blood flow and oxygenation disturbances that impair cerebral cortex growth and cause life-long cognitive and learning disabilities. We investigated the fate of subplate neurons (SPNs), which are a master regulator of brain development that plays critical roles in establishing cortical connections to other brain regions. We utilized a preterm fetal sheep model that reproduces key features of brain injury in human preterm survivors. We analyzed the responses of fetal SPNs to transient disturbances in fetal oxygenation. We discovered that SPNs are surprisingly resistant to cell death from low oxygen states, but acquire chronic structural and functional changes that suggest new strategies to prevent learning problems in children and adults that survive preterm birth.

Authors: Evelyn McClendon, Daniel C. Shaver, Kiera Degener-O'Brien, Xi Gong, Thuan Nguyen, Anna Hoerder-Suabedissen, Zoltán Molnár, Claudia Mohr, Ben D. Richardson, David J. Rossi and Stephen A. Back

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Nov 7, 2017   Fetal Timeline   Maternal Timeline   News   News Archive

"This brief exposure to low oxygen occurs frequently in preterm babies receiving care in a neonatal intensive care unit." explains Stephen Back MD PhD, Oregon Health & Science University.

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