Mechanisms for Programmed Cell Death in the Nervous System of a Moth

  1. Gregory Bock Organizer and
  2. Maeve O'Connor
  1. Susan E. Fahrbach and
  2. James W. Truman

Published Online: 28 SEP 2007

DOI: 10.1002/9780470513422.ch5

Ciba Foundation Symposium 126 - Selective Neuronal Death

Ciba Foundation Symposium 126 - Selective Neuronal Death

How to Cite

Fahrbach, S. E. and Truman, J. W. (2007) Mechanisms for Programmed Cell Death in the Nervous System of a Moth, 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.ch5

Author Information

  1. Department of Zoology, NJ-15, University of Washington, Seattle, WA 98195, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471910923

Online ISBN: 9780470513422

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Keywords:

  • programmed cell death;
  • manduca sexta;
  • cycloheximide;
  • actinomycin-D;
  • MN-12 cells

Summary

In the moth Manduca sexta 50% of the abdominal motor neurons and interneurons die during the first days after the adult emerges. Although the dying motor neurons innervate larval muscles that also die at this time, the death of the neurons has been shown to be a direct response to an endocrine signal, the decline in ecdysteroids that occurs at the end of metamorphosis. The response to the withdrawal of the hormone apparently requires new synthesis of RNA and protein, as actinomycin-D and cycloheximide can prevent neuronal death. This selective neuronal death probably results from changes in gene activation. The fixed spatial and temporal pattern of neuronal death, however, suggests that trophic interactions among neurons may also be involved. Current work is focused on the fate of a pair of motor neurons, the MN-12 cells, in the third abdominal ganglion. Isolation of this ganglion from the thoracic ganglia can prevent the death of these cells at the time when they would normally die in response to removal of ecdysteroids. The factors mediating this effect may act in concert with the ecdysteroid decline to specify the exact time of death for individual neurons.