Repair of Neocortex in a Model of Cortical Dysplasia

Abstract

Our lab developed an animal model to elucidate factors associated with abnormal neocortical development and to attempt repair of cortical dysgenesis. We disrupt corticogenesis using an anti-mitotic methylazoxy methanol (MAM), which inhibits mitosis for several hours. The effects of MAM on neocortical development are assessed during early (embryonic day 24; E24) and late (E33) corticogenesis in ferrets. These animals have protracted cortical development with neurogenesis and migration continuing postnatally. MAM treatment on E24 leads to disorganized cortical laminae, abnormal radial morphology, precocious differentiation of radial glia, and dispersal of Cajal Retzius cells. MAM treatment on E33 leads to less severe effects including diminished layer 4, widespread termination of thalamocortical afferents, and abnormal distribution of GABAA-alpha receptors.

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Document Details

Document Type
Technical Report
Publication Date
Mar 27, 2007
Accession Number
AD1014064

Entities

People

  • Alisa W. Schaefer

Organizations

  • Uniformed Services University of the Health Sciences

Tags

DTIC Thesaurus Topics

  • Brain
  • Cell Physiological Processes
  • Cells
  • Embryos
  • Genetics
  • Health Services
  • Nervous System Malformations
  • Neurodegeneration
  • Neurons
  • Neurosciences
  • Peptide Growth Factors
  • Peptides
  • Proteins
  • Sodium Compounds
  • Stem Cells

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics
  • Neuroscience