The effects of natural cell loss on the regularity of the retinal cholinergic arrays

J Neurosci. 2000 Feb 1;20(3):RC60. doi: 10.1523/JNEUROSCI.20-03-j0005.2000.

Abstract

The retina provides a paradigmatic example of the modularity of neuronal circuitry. Different cells are stacked in layers, and neurons of the same type are commonly regularly spaced within their layer. Although the orderly arrays formed by homotypic neurons provide the basis for parallel processing, the mechanisms responsible for regular cell spacing are just beginning to be elucidated. All the developing retinal arrays for which early markers have been identified are regular before being complete. This indicates that the positional constraints controlling mosaic formation are active at times when cell genesis, migration, and death also occur in the retina. To begin investigating how these different processes are coordinated, we have focused here on the effects of cell death on the spatial organization of the two rat cholinergic mosaics, the only arrays for which the development of spatial ordering has been described quantitatively to date. We have chosen an age interval when new cell genesis is over and death predominantly or nearly exclusively controls cell number in one of these array. We found that the regularity of this array is not improved by the loss of cells occurring in this age period. Rather, death appears to be largely independent of cell position.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Death
  • Choline O-Acetyltransferase / metabolism*
  • Eye Proteins / metabolism
  • Homeodomain Proteins / metabolism
  • Immunohistochemistry
  • LIM-Homeodomain Proteins
  • Microscopy, Confocal
  • Nerve Tissue Proteins / metabolism
  • Neurons / cytology*
  • Neurons / metabolism
  • Rats
  • Rats, Long-Evans
  • Retina / cytology*
  • Retina / metabolism
  • Transcription Factors

Substances

  • Eye Proteins
  • Homeodomain Proteins
  • LIM-Homeodomain Proteins
  • Nerve Tissue Proteins
  • Transcription Factors
  • insulin gene enhancer binding protein Isl-1
  • Choline O-Acetyltransferase