Elsevier

Neuroscience

Volume 62, Issue 1, September 1994, Pages 291-305
Neuroscience

Expression of polysialylated neural cell adhesion molecule by proliferating cells in the subependymal layer of the adult rat, in its rostral extension and in the olfactory bulb

https://doi.org/10.1016/0306-4522(94)90333-6Get rights and content

Abstract

The highly sialylated isoform of the neural cell adhesion molecule is thought to be expressed predominantly in the developing nervous system, where it is implicated in a variety of dynamic events linked to neural morphogenesis. It has become increasingly evident, however, that this “embryonic” neural cell adhesion molecule isoform continues to be expressed in certain adult neuronal systems, and in particular, in those that can undergo structural plasticity. In the present study, we performed light microscopic immunocytochemistry with an antibody specific for polysialylated neural cell adhesion molecule and confirmed our earlier observations [Bonfanti L. et al. (1992) Neuroscience 49, 419–436] showing polysialylated neural cell adhesion molecule-immunoreactive cells in the subependymal layer of the lateral ventricle of the adult rat, a region where cell proliferation continues into the postnatal period. In addition, we used an antibody raised against the proliferating cell nuclear antigen and found that proliferating cells continue to be visible in this area, even in the adult. Double immunolabeling showed that many of these newly generated cells displayed high polysialylated neural cell adhesion molecule immunoreactivity. Cells from a portion of the subependymal layer migrate to the olfactory bulb and contribute to the continual replacement of its granule neurons [Luskin M.B. (1993) Neuron 11, 173–189]. We found polysialylated neural cell adhesion molecule-immunoreactive cells all along the pathway purported to be followed by the newly generated cells to their final destination and in neurons corresponding to granular and periglomerular cells in the olfactory bulb.

Our present observations thus support the contention that polysialylation is a feature of neurons capable of dynamic change and may contribute to the molecular mechanisms permitting cell proliferation and migration not only during development but also in the adult.

References (44)

  • AltaianJ.

    Autoradiographic and histological studies of postnatal neurogenesis. IV. Cell proliferation and migration in the anterior forebrain, with special reference to persisting neurogenesis in the olfactory bulb

    J. comp. Neurol.

    (1969)
  • BayerS.A.

    3H-Thymidine-radiographic studies of neurogenesis in the rat olfactory bulb

    Expl Brain Res.

    (1983)
  • BoisseauS. et al.

    Analysis of high PSA N-CAM expression during mammalian spinal cord and peripheral nervous system development

    Development

    (1991)
  • Boulder Committee

    Embryonic vertebrate central nervous system: revised terminology

    Anat. Rec.

    (1970)
  • CremerH. et al.

    Inactivation of the N-CAM gene in mice results in size reduction of the olfactory bulb and deficits in spatial learning

    Nature

    (1994)
  • EdelmanG.M.

    Modulation of cell adhesion during induction, histogenesis, and perinatal development of the nervous system

    A. Rev. Neurosci.

    (1984)
  • EdelmanG.M. et al.

    Cell adhesion molecules in neural morphogenesis

  • EdelmanG.M. et al.

    Cell adhesion molecules: implications for a molecular histology

    A. Rev. Biochem.

    (1991)
  • GlobusJ.H. et al.

    The subependymal cell plate (matrix) and its relationship to brain tumors of the ependymal type

    J. Neuropath.

    (1944)
  • GraziadeiP.P.C. et al.

    Continuous nerve cell renewal in the olfactory system

  • HallP.A. et al.

    Proliferating cell nuclear antigen (PCNA) immunolocalization in paraffin sections: an index of cell proliferation with evidence of deregulated expression in some neoplasms

    J. Path.

    (1990)
  • HindsJ.W.

    Autoradiographic study of histogenesis in the mouse olfactory bulb. II. Cell proliferation and migration

    J. comp. Neurol.

    (1968)
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