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Functional Deficit and Recovery of Developing Sensorimotor Networks following Neonatal Hypoxic-Ischemic Injury in the Rat

Quairiaux, Charles ; Sizonenko, Stéphane V. ; Mégevand, Pierre ; Michel, Christoph M. ; Kiss, Jozsef Z.

In: Cerebral Cortex, 2010, vol. 20, no. 9, p. 2080-2091

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    Title
    • Functional Deficit and Recovery of Developing Sensorimotor Networks following Neonatal Hypoxic-Ischemic Injury in the Rat
    Author
    • Quairiaux, Charles. Faculty of Medicine, Department of Fundamental Neurosciences, University of Geneva, 1211 Geneva, Switzerland
    • Sizonenko, Stéphane V.. Division of development and Growth, Department of Child and Adolescent
    • Mégevand, Pierre. Functional Brain Mapping Laboratory, Department of Clinical Neuroscience, Geneva University Hospital, 1211 Geneva, Switzerland
    • Michel, Christoph M.. Functional Brain Mapping Laboratory, Department of Clinical Neuroscience, Geneva University Hospital, 1211 Geneva, Switzerland
    • Kiss, Jozsef Z.. Faculty of Medicine, Department of Fundamental Neurosciences, University of Geneva, 1211 Geneva, Switzerland
    Document Type
    • Postprint
    Language
    • English
    Published in
    • Cerebral Cortex, 2010, vol. 20, no. 9, p. 2080-2091. Oxford University Press
    Other Version
    OAI-PMH Identifier
    • oai:doc.rero.ch:302983
    Summary
    Neonatal hypoxia-ischemia (HI) is the most important cause of brain injury in the newborn. Here we studied structural alterations and functional perturbations of developing large-scale sensorimotor cortical networks in a rat model of moderate HI at postnatal day 3 (P3). At the morphological level, HI led to a disorganized barrel pattern in the somatosensory cortex without detectable histological changes in the motor cortex. Functional effects were addressed by means of epicranial mapping of somatosensory-evoked potentials (SEPs) during the postischemic recovery period. At P10, SEPs were immature and evoked activity was almost restricted to the somatosensory and motor cortices of the contralateral hemisphere. Peak and topographic analyses of epicranial potentials revealed that responses were profoundly depressed in both sensory and motor areas of HI-lesioned animals. At the end of the postnatal period at P21, responses involved networks in both hemispheres. SEP amplitude was still depressed in the injured sensory region, but it completely recovered in the motor area. These results suggest a process of large-scale network plasticity in sensorimotor circuits after perinatal ischemic injury. The model provides new perspectives for investigating the temporal and spatial characteristics of the recovery process following HI and eventually developing therapeutic interventions