Remodelling of Early Axonal Projections Through the Selective Elimination of Neurons and Long Axon Collaterals

  1. Gregory Bock Organizer and
  2. Maeve O'Connor
  1. Dennis D.M. O'Leary

Published Online: 28 SEP 2007

DOI: 10.1002/9780470513422.ch8

Ciba Foundation Symposium 126 - Selective Neuronal Death

Ciba Foundation Symposium 126 - Selective Neuronal Death

How to Cite

O'Leary, D. D.M. (2007) Remodelling of Early Axonal Projections Through the Selective Elimination of Neurons and Long Axon Collaterals, in Ciba Foundation Symposium 126 - Selective Neuronal Death (eds G. Bock and M. O'Connor), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470513422.ch8

Author Information

  1. Developmental Neurobiology Laboratory, The Salk Institute for Biological Studies, P.O. Box 85800, San Diego, CA 92138, USA

  1. Department of Neurosurgery, Box 8057, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471910923

Online ISBN: 9780470513422

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Keywords:

  • axonal projections remodelling;
  • selective elimination;
  • axon collaterals;
  • ganglion cells;
  • retinofugal projection

Summary

Studies using neuroanatomical techniques have shown that the connections characteristic of the mature vertebrate brain are brought about by a considerable refinement of the projections initially established during development. The selective loss of neurons and long axon collaterals plays a major role in this remodelling process as illustrated in the development of the retina and cortex of the rat. In the retina, two-thirds of the initial population of ganglion cells (RGCs) die early. This loss serves to remove selectively RGCs that make erroneous axonal projections, including those which project to an incorrect target, to an inappropriate part of a correct target, or to the wrong side of the brain. Studies using the sodium channel blocker, tetrodotoxin, suggest that in rats the selective elimination of erroneously projecting RGCs is based, in part, on patterns of impulse activity. In the cortex a different mechanism is illustrated. All neocortical areas initially give rise to callosal and pyramidal tract axons but through a process of selective collateral elimination not involving cell death these projections assume the limited distributions seen in adult rats. Manipulations resulting in the maintenance of such long collaterals suggest that their removal is functionally and locally determined. In contrast to error elimination, this phenomenon of collateral elimination may be a developmental strategy for generating connectional diversity while limiting the amount of information required for the regional specification of the cortex.