Mouse embryonic retina delivers information controlling cortical neurogenesis

PLoS One. 2010 Dec 8;5(12):e15211. doi: 10.1371/journal.pone.0015211.

Abstract

The relative contribution of extrinsic and intrinsic mechanisms to cortical development is an intensely debated issue and an outstanding question in neurobiology. Currently, the emerging view is that interplay between intrinsic genetic mechanisms and extrinsic information shape different stages of cortical development. Yet, whereas the intrinsic program of early neocortical developmental events has been at least in part decoded, the exact nature and impact of extrinsic signaling are still elusive and controversial. We found that in the mouse developing visual system, acute pharmacological inhibition of spontaneous retinal activity (retinal waves-RWs) during embryonic stages increase the rate of corticogenesis (cell cycle withdrawal). Furthermore, early perturbation of retinal spontaneous activity leads to changes of cortical layer structure at a later time point. These data suggest that mouse embryonic retina delivers long-distance information capable of modulating cell genesis in the developing visual cortex and that spontaneous activity is the candidate long-distance acting extrinsic cue mediating this process. In addition, these data may support spontaneous activity to be a general signal coordinating neurogenesis in other developing sensory pathways or areas of the central nervous system.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bromodeoxyuridine / pharmacology
  • Central Nervous System / embryology
  • Cerebral Cortex / embryology*
  • Colforsin / pharmacology
  • Gene Expression Regulation, Developmental*
  • Immunohistochemistry / methods
  • In Situ Hybridization
  • Injections, Intraocular
  • Ki-67 Antigen / biosynthesis
  • Mice
  • Models, Biological
  • Retina / embryology*
  • Time Factors
  • Visual Cortex / embryology

Substances

  • Ki-67 Antigen
  • Colforsin
  • Bromodeoxyuridine