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@article{rodriguez-duboc2022,
author = {Rodriguez-Duboc, Agalic and Leroux, Sarah and Arabo, Arnaud
and Basille-Duguay, Magali and Vaudry, David and Burel, Delphine},
title = {Intermittent Hypoxia in a Mouse Model of Apnea of Prematurity
Leads to a Retardation of Cerebellar Development and Long-Term
Functional Deficits},
journal = {Cell \& Bioscience},
volume = {12},
number = {1},
date = {2022-09-06},
url = {https://cellandbioscience.biomedcentral.com/articles/10.1186/s13578-022-00869-5},
doi = {10.1186/s13578-022-00869-5},
issn = {2045-3701},
langid = {en},
abstract = {**Background:** Apnea of prematurity (AOP) is caused by
respiratory control immaturity and affects nearly 50\% of premature
newborns. This pathology induces perinatal intermittent hypoxia
(IH), which leads to neurodevelopmental disorders. The impact on the
brain has been well investigated. However, despite its functional
importance and immaturity at birth, the involvement of the
cerebellum remains poorly understood. Therefore, this study aims to
identify the effects of IH on cerebellar development using a mouse
model of AOP consisting of repeated 2-min cycles of hypoxia and
reoxygenation over 6 h and for 10 days starting on postnatal day 2
(P2). **Results:** At P12, IH-mouse cerebella present higher
oxidative stress associated with delayed maturation of the
cerebellar cortex and decreased dendritic arborization of Purkinje
cells. Moreover, mice present with growth retardation and motor
disorders. In response to hypoxia, the developing cerebellum
triggers compensatory mechanisms resulting in the unaltered
organization of the cortical layers from P21 onwards. Nevertheless,
some abnormalities remain in adult Purkinje cells, such as the
dendritic densification, the increase in afferent innervation, and
axon hypomyelination. Moreover, this compensation seems insufficient
to allow locomotor recovery because adult mice still show motor
impairment and significant disorders in spatial learning.
**Conclusions:** All these findings indicate that the cerebellum is
a target of intermittent hypoxia through alterations of
developmental mechanisms leading to long-term functional deficits.
Thus, the cerebellum could contribute, like other brain structures,
to explaining the pathophysiology of AOP.}
}
For attribution, please cite this work as:
Rodriguez-Duboc, A., Leroux, S., Arabo, A., Basille-Duguay, M., Vaudry,
D., & Burel, D. (2022). Intermittent hypoxia in a mouse model of
apnea of prematurity leads to a retardation of cerebellar development
and long-term functional deficits. Cell & Bioscience,
12(1). https://doi.org/10.1186/s13578-022-00869-5