A new view of early cortical development

Biochem Pharmacol. 1998 Dec 1;56(11):1403-9. doi: 10.1016/s0006-2952(98)00209-3.

Abstract

Recently, several genes that regulate the development of the cerebral cortex and are potential pharmacological targets have been cloned. Reelin, an extracellular matrix glycoprotein secreted by Cajal-Retzius cells in the marginal zone, instructs the radial organization of the cortical plate. The response of cortical plate cells to reelin requires the tyrosine kinase adaptor disabled-1 (Dab1). Cyclin-dependent kinase 5 and its activator p35 are necessary for the development of the cortical plate, probably at a later stage than reelin/Dab1. The transcription factor Tbr-1 is essential for differentiation of preplate and Cajal-Retzius cells and for formation of thalamocortical connections, while D1x-1/2 are required for tangential migration. Some neurotrophin systems such as neurotrophin 4, brain-derived neurotrophic factor, and neuregulin and its receptor ErbB are also thought to assist in the regulation of cortical development. In addition, a few genes implicated in human cortical dysplasias have been characterized. LIS1 encodes a protein related to platelet-activating factor acetyl hydrolase that is defective in lissencephaly-1 of the Miller-Dieker type, while the double cortex malformation is related to mutations of a new gene dubbed doublecortn.

Publication types

  • Review

MeSH terms

  • Animals
  • Cerebral Cortex / abnormalities
  • Cerebral Cortex / growth & development*
  • Cerebral Cortex / metabolism*
  • Cyclin-Dependent Kinases / metabolism
  • Growth Substances / physiology
  • Humans
  • Mammals
  • Mice
  • Mice, Neurologic Mutants
  • Models, Neurological
  • Reelin Protein
  • Transcription Factors / metabolism

Substances

  • Growth Substances
  • Reelin Protein
  • Transcription Factors
  • Cyclin-Dependent Kinases
  • RELN protein, human
  • Reln protein, mouse