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  1. Artikel ; Online: Neonatal Hyperoxia Perturbs Neuronal Development in the Cerebellum.

    Scheuer, Till / Sharkovska, Yuliya / Tarabykin, Victor / Marggraf, Katharina / Brockmöller, Vivien / Bührer, Christoph / Endesfelder, Stefanie / Schmitz, Thomas

    Molecular neurobiology

    2017  Band 55, Heft 5, Seite(n) 3901–3915

    Abstract: Impaired postnatal brain development of preterm infants often results in neurological deficits. Besides pathologies of the forebrain, maldeveolopment of the cerebellum is increasingly recognized to contribute to psychomotor impairments of many former ... ...

    Abstract Impaired postnatal brain development of preterm infants often results in neurological deficits. Besides pathologies of the forebrain, maldeveolopment of the cerebellum is increasingly recognized to contribute to psychomotor impairments of many former preterm infants. However, causes are poorly defined. We used a hyperoxia model to define neonatal damage in cerebellar granule cell precursors (GCPs) and in Purkinje cells (PCs) known to be essential for interaction with GCPs during development. We exposed newborn rats to 24 h 80% O
    Mesh-Begriff(e) Animals ; Animals, Newborn ; Cell Count ; Cell Death/genetics ; Cell Proliferation/genetics ; Cerebellum/growth & development ; Cerebellum/pathology ; Dendrites/metabolism ; Gene Expression Regulation, Developmental ; Hedgehog Proteins/metabolism ; Hyperoxia/genetics ; Hyperoxia/pathology ; Neurogenesis ; Neurons/metabolism ; Neurons/pathology ; Purkinje Cells/metabolism ; Rats, Wistar
    Chemische Substanzen Hedgehog Proteins
    Sprache Englisch
    Erscheinungsdatum 2017-05-25
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-017-0612-5
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Oligodendroglial maldevelopment in the cerebellum after postnatal hyperoxia and its prevention by minocycline.

    Scheuer, Till / Brockmöller, Vivien / Blanco Knowlton, Marissa / Weitkamp, Jörn-Hendrik / Ruhwedel, Torben / Mueller, Susanne / Endesfelder, Stefanie / Bührer, Christoph / Schmitz, Thomas

    Glia

    2015  Band 63, Heft 10, Seite(n) 1825–1839

    Abstract: According to recent research, brain injury after premature birth often includes impaired growth of the cerebellum. However, causes of cerebellar injury in this population are poorly understood. In this study, we analyzed whether postnatal hyperoxia ... ...

    Abstract According to recent research, brain injury after premature birth often includes impaired growth of the cerebellum. However, causes of cerebellar injury in this population are poorly understood. In this study, we analyzed whether postnatal hyperoxia perturbs white matter development of the cerebellum, and whether cerebellar glial damage can be prevented by minocycline. We used a hyperoxia model in neonatal rats providing 24 h exposure to fourfold increased oxygen concentration (80% O2) from P6 to P7, followed by recovery in room air until P9, P11, P15, P30. Injections with minocycline were performed at the beginning and 12 h into hyperoxia exposure. Hyperoxia induced oxidative stress in the cerebellum at P7 as evidenced by increased nitrotyrosine concentrations. Numbers of proliferating, NG2+Ki67+ oligodendroglial precursor cells were decreased at P7 after hyperoxia and at P11 following recovery in room air. Numbers of mature, CC1+ oligodendrocytes were diminished in recovering hyperoxia rats, and myelin basic protein expression was still decreased at P30. Electron microscopy analysis of myelinated fibers at P30 revealed thinner myelin sheath after hyperoxia. Long-term injury of the cerebellum by neonatal hyperoxia was confirmed by reduced volumes in MRI measurements at P30. In response to 80% O2, expression of platelet-derived growth factor (PDGF)-A was largely reduced in cerebellar tissue and also in cultured cerebellar astrocytes. Treatment with minocycline during hyperoxia prevented oxidative stress, attenuated oligodendroglial injury, and improved astroglial PDGF-A levels. In conclusion, early hyperoxia causes white matter damage in the cerebellum with astroglial dysfunction being involved, and both can be prevented by treatment with minocycline. Neonatal exposure to hyperoxia causes hypomyelination of the cerebellum. Reduced astroglial growth factor production but not microglial inflammation seems to contribute to oligodendroglial damage, and minocycline rescues oligodendroglia development in the cerebellum after hyperoxia.
    Mesh-Begriff(e) Age Factors ; Animals ; Animals, Newborn ; Apoptosis/drug effects ; Cell Communication/drug effects ; Cell Death/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Cerebellum/drug effects ; Cerebellum/growth & development ; Cerebellum/pathology ; Cytokines/metabolism ; Disease Models, Animal ; Embryo, Mammalian ; Hyperoxia/pathology ; Hyperoxia/prevention & control ; Minocycline/therapeutic use ; Nerve Tissue Proteins/metabolism ; Oligodendroglia/drug effects ; Oligodendroglia/pathology ; Oligodendroglia/ultrastructure ; Oxidative Stress/drug effects ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Stem Cells/drug effects
    Chemische Substanzen Cytokines ; Nerve Tissue Proteins ; Minocycline (FYY3R43WGO)
    Sprache Englisch
    Erscheinungsdatum 2015-10
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 639414-0
    ISSN 1098-1136 ; 0894-1491
    ISSN (online) 1098-1136
    ISSN 0894-1491
    DOI 10.1002/glia.22847
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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