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Soluble KDI domain of γ1 laminin protects adult hippocampus from excitotoxicity of kainic acid

Authors

  • Markus Wiksten,

    1. The Brain Laboratory, Department of Biological and Environmental Sciences (Physiology), University of Helsinki, Helsinki, Finland
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  • Antti Väänänen,

    1. The Brain Laboratory, Department of Biological and Environmental Sciences (Physiology), University of Helsinki, Helsinki, Finland
    2. Institute of Biomedicine (Pharmacology), Biomedicum Helsinki, Helsinki, Finland
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  • Ron Liebkind,

    1. The Brain Laboratory, Department of Biological and Environmental Sciences (Physiology), University of Helsinki, Helsinki, Finland
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  • Pekka Rauhala,

    1. Institute of Biomedicine (Pharmacology), Biomedicum Helsinki, Helsinki, Finland
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  • Päivi Liesi

    Corresponding author
    1. The Brain Laboratory, Department of Biological and Environmental Sciences (Physiology), University of Helsinki, Helsinki, Finland
    2. Johnnie B. Byrd Sr. Alzheimer's Center and Research Institute, Tampa, Florida
    • The Brain Laboratory, Department of Biological and Environmental Sciences (Physiology), University of Helsinki, Biocenter 3, PO Box 65 (Viikinkaari 1), 00014 University of Helsinki, Helsinki, Finland
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Abstract

Recent data indicate that the soluble KDI domain of γ1 laminin promotes survival and neurite outgrowth of human central neurons in vitro (Liebkind et al.[2003] J Neurosci Res 73:637–643), and seems to neutralize both glia- and myelin-derived signals that hamper regeneration in the central nervous system (CNS) of adult mammals. We show that damage of adult rat neocortical and hippocampal areas by a stereotaxic injection of kainic acid (KA) is prevented by a preceding injection of the soluble KDI domain. In the presence of the KDI domain, both neocortical and hippocampal areas show extensive gliosis but have viable neurons and glial cells, which are absent and the areas fully destroyed after injection of KA alone. This result indicates that the KDI domain of the γ1 laminin protects the CNS against excitotoxic insults and promotes survival of both neurons and glial cells. The KDI domain may thus be a potential drug to prevent CNS damage induced by neurodegenerative disorders, mechanical injury, or ischemia. © 2004 Wiley-Liss, Inc.

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