4.5 Article

Morphological Differences Between Wild-Type and Transgenic Superoxide Dismutase 1 Lumbar Motoneurons in Postnatal Mice

期刊

JOURNAL OF COMPARATIVE NEUROLOGY
卷 511, 期 3, 页码 329-341

出版社

WILEY-LISS
DOI: 10.1002/cne.21818

关键词

ALS; dendrites; neurodegenerative disease; abnormal branching; spinal cord

资金

  1. Centre National de la Recherche Scientifique (CNRS)
  2. Association Francaise contre les Myopathies [11117]
  3. Association pour la recherche sur la Sclerose Laterale Amyotrophique et autres maladies du motoneurone

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Quantitative analysis of the dendritic arborizations of wild-type (WT) and superoxide dismutase 1 (SOD1) postnatal mouse motoneurons was performed following intracellular staining and 3D reconstructions with Neurolucida system. The population of lumbar motoneurons was targeted in the caudal part of the L5 segment, and all labeled motoneurons were located within the same ventrolateral pool. Despite the similar size of the soma and the mean diameter of primary dendrites, the dendritic arborizations of the WT and SOD1 motoneurons showed significant differences in terms of their morphometric parameters. The metric and topological parameters of dendrites show that the total dendritic length and surface area and total number of segments, branching nodes, and tips per motoneuron were significantly higher in SOD1 motoneurons. Our main finding concerns a proliferation of dendritic branches starting at about 100 mu m from the soma in the SOD1 motoneurons. However, the longest and mean dendritic paths from soma to terminations were similar, giving a comparable envelope of the dendritic fields. Indeed, the SOD1 motoneurons were larger as a result of abnormal branching. The results suggest that a defect in pruning mechanisms occurs during this developmental period. The abnormal growth of the dendritic arborizations and the reduced excitability of postnatal SOD1 motoneurons could be a neuroprotective response and would represent an early compensatory mechanism against the activity-induced toxicity. J. Comp. Neurol. 511:329-341, 2008. (c) 2008 Wiley-Liss, Inc.

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