Deficits of brainstem and spinal cord functions after neonatal hypoxia–ischemia in mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-03-11

AUTHORS

Blandine Bellot, Julie Peyronnet-Roux, Catherine Gire, Umberto Simeoni, Laurent Vinay, Jean-Charles Viemari

ABSTRACT

Background: Perinatal cerebral hypoxia–ischemia (HI) can lead to severe neurodevelopmental disorders. Studies in humans and animal models mainly focused on cerebral outcomes, and little is known about the mechanisms that may affect the brainstem and the spinal cord. Dysfunctions of neuromodulatory systems, such as the serotonergic (5-HT) projections, critical for the development of neural networks, have been postulated to underlie behavioral and motor deficits, as well as metabolic changes.Methods:The aim of this study was to investigate brainstem and spinal cord functions by means of plethysmography and sensorimotor tests in a neonatal Rice–Vanucci model of HI in mice. We also evaluated bioaminergic contents in central regions dedicated to the motor control of autonomic functions.Results:Mice with cerebral infarct expressed motor disturbances and had a lower body weight and a decreased respiratory frequency than SHAM, suggesting defects of brainstem neural network involved in the motor control of feeding, suckling, swallowing, and respiration. Moreover, our study revealed changes of monoamine and amino acid contents in the brainstem and the spinal cord of HI mice.Conclusion:Our results suggest that monoaminergic neuromodulation plays an important role in the physiopathology of HI brain injury that may represent a good therapeutic target. More... »

PAGES

723-730

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/pr.2014.42

DOI

http://dx.doi.org/10.1038/pr.2014.42

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1048279788

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24618565


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