ArticleAnnals of neurology2014
Unmyelinated axon loss with postnatal hypertonia after fetal hypoxia.
Article in Annals of neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Modeling cerebral palsy in animals.Developmental medicine and child neurology · 2026Review
- Circadian patterns of heart rate variability in fetal sheep after hypoxia-ischaemia: A biomarker of evolving brain injury.The Journal of physiology · 2024Article
- The RhoB p.S73F mutation leads to cerebral palsy through dysregulation of lipid homeostasis.EMBO molecular medicine · 2024Article
- Article
- Recent Investigations on Neurotransmitters' Role in Acute White Matter Injury of Perinatal Glia and Pharmacotherapies-Glia Dynamics in Stem Cell Therapy.Molecular neurobiology · 2022Review
- Earlier preterm birth is associated with a worse neurocognitive outcome in a rabbit model.PloS one · 2021Article
- Experimentally Induced Sepsis Causes Extensive Hypomyelination in the Prefrontal Cortex and Hippocampus in Neonatal Rats.Neuromolecular medicine · 2020Article
- Long-term neurological effects of neonatal caffeine treatment in a rabbit model of preterm birth.Pediatric research · 2020Article
- Animal models of developmental motor disorders: parallels to human motor dysfunction in cerebral palsy.Journal of neurophysiology · 2019Article
- Glial Cell AMPA Receptors in Nervous System Health, Injury and Disease.International journal of molecular sciences · 2019Review
- Supraphysiological Levels of Oxygen Exposure During the Neonatal Period Impairs Signaling Pathways Required for Learning and Memory.Scientific reports · 2018Article
- Spinal Hyper-Excitability and Altered Muscle Structure Contribute to Muscle Hypertonia in Newborns After Antenatal Hypoxia-Ischemia in a Rabbit Cerebral Palsy Model.Frontiers in neurology · 2018Article
- Spinal cord injury in hypertonic newborns after antenatal hypoxia-ischemia in a rabbit model of cerebral palsy.Experimental neurology · 2017Article
- Concurrent decrease of brain white matter tracts' thicknesses and fractional anisotropy after antenatal hypoxia-ischemia detected with tract-based spatial statistics analysis.Journal of magnetic resonance imaging : JMRI · 2017Article
- Controversies in preterm brain injury.Neurobiology of disease · 2016Review
- Article
- Extending the duration of hypothermia does not further improve white matter protection after ischemia in term-equivalent fetal sheep.Scientific reports · 2016Article
- Prenatal ischemia deteriorates white matter, brain organization, and function: implications for prematurity and cerebral palsy.Developmental medicine and child neurology · 2016Review
- Magnetic resonance imaging anatomy of the rabbit brain at 3 T.Acta veterinaria Scandinavica · 2015Article
- Premyelinated central axons express neurotoxic NMDA receptors: relevance to early developing white-matter injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveWhite matter (WM) injury due to myelination defects is believed to be responsible for the motor deficits seen in cerebral palsy. We tested the hypothesis that the predominant injury is to functional electrical connectivity in unmyelinated WM fibers by conducting a longitudinal study of central WM tracts in newborn rabbit kits with hypertonia in our model of cerebral palsy.
methodsPregnant rabbits at 70% gestation underwent 40-minute uterine ischemia. Motor deficits in newborn kits, including muscle hypertonia, were assessed by neurobehavioral testing. Major central WM tracts, including internal capsule, corpus callosum, anterior commissure, and fimbria hippocampi, were investigated for structural and functional injury using diffusion tensor magnetic resonance imaging (MRI), electrophysiological recordings of fiber conductivity in perfused brain slices, electron microscopy, and immunohistochemistry of oligodendrocyte lineage.
resultsMotor deficits were observed on postnatal day 1 (P1) when WM tracts were unmyelinated. Myelination occurred later and was obvious by P18. Hypertonia was associated with microstructural WM injury and unmyelinated axon loss at P1, diagnosed by diffusion tensor MRI and electron microscopy. Axonal conductivity from electrophysiological recordings in hypertonic P18 kits decreased only in unmyelinated fibers, despite a loss in both myelinated and unmyelinated axons.
interpretationMotor deficits in cerebral palsy were associated with loss of unmyelinated WM tracts. The contribution of injury to myelinated fibers that was observed at P18 is probably a secondary etiological factor in the motor and sensory deficits in the rabbit model of cerebral palsy.
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