CRMP3 is required for hippocampal CA1 dendritic organization and plasticity

    Authors

    T. T. Quach; G. Massicotte; M. F. Belin; J. Honnorat; E. R. Glasper; A. C. Devries; L. B. Jakeman; M. Baudry; A. M. Duchemin;P. E. Kolattukudy

    Comments

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    Abbreviated Journal Title

    Faseb J.

    Keywords

    Golgi analysis; gene targeting; neurite outgrowth; LTP; RESPONSE MEDIATOR PROTEINS; LONG-TERM POTENTIATION; GROWTH CONE; NEURONS; ACTIN; SYSTEM; MICE; PHOSPHORYLATION; INVOLVEMENT; EXPRESSION; Biochemistry & Molecular Biology; Biology; Cell Biology

    Abstract

    In vitro studies have pointed to the collapsin response mediator proteins (CRMPs) as key regulators of neurite outgrowth and axonal differentiation. CRMP3 is expressed mostly in the nervous system during development but remains at high levels in the hippocampus of adults. To explore CRMP3 function in vivo, we generated mice with targeted disruption of the CRMP3 gene. Immunohistochemistry and Golgi staining of CA1 showed abnormal dendrite and spine morphogenesis in the hippocampus of CRMP3-deficient mice. Apical dendrites displayed an increase in undulation and a reduction in length and branching points. Basal dendrites also exhibited a reduction in length with an alteration in soma stem distribution and an increased number of thick dendrites localized in stratum oriens (SO). Long-term potentiation (LTP) was impaired in this area. These data indicate an important role for CRMP3 in dendrite arborization, guide-posts navigation, and neuronal plasticity.

    Journal Title

    Faseb Journal

    Volume

    22

    Issue/Number

    2

    Publication Date

    1-1-2008

    Document Type

    Article

    Language

    English

    First Page

    401

    Last Page

    409

    WOS Identifier

    WOS:000252822600010

    ISSN

    0892-6638

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