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|Title:||The regulation of motoneuron survival in the tobacco hornworm, Manduca sexta|
|Author(s):||Choi, Mikyung Kim|
|Doctoral Committee Chair(s):||Fahrbach, Susan E.|
|Department / Program:||Entomology|
|Degree Granting Institution:||University of Illinois at Urbana-Champaign|
Biology, Animal Physiology
|Abstract:||The death of half of the neurons in the abdominal nervous system accompanies the emergence of the adult Manduca sexta moth. The cell loss is regulated both by hemolymph concentrations of a steroid hormone, 20-hydroxyecdysone, and in the case of the MN-12 motoneurons, by actions exerted by neighboring ganglia.
To study the interactions between the pterothoracic ganglion and the first unfused abdominal ganglion, A3, I have chosen motoneuron-12 (MN-12) as a model system. I have developed culture conditions in which the pattern of cell death parallels that seen in intact moths. Using this in vitro system, I have replicated the sparing effect on MN-12 of cutting the ventral nerve cord anterior to the first unfused abdominal ganglion. This effect was most readily seen when the cultures were initiated between 21 and 24 h after adult ecdysis, suggesting that this period may be the "window of sensitivity" to a neuron-killing factor. Results also suggest the existence of a soluble neuron-killing factor in the M. sexta nervous system.
In order to test the hypothesis that this programmed cell death is an active process regulated by 20-hydroxyecdysone, I tested the effects of RNA and protein synthesis inhibitors and the effect of the steroid on the survival of the D-IV and MN-12 motoneurons. The death of neurons was markedly reduced by treatment with actinomycin D and cycloheximide. The ability of actinomycin D to prevent neuronal death waned at the same time at which replacement of the steroid hormone could no longer block neuronal death. This suggests that the steroid commitment point represents the time at which the genes that mediate cell death are transcribed. Cycloheximide remained effective in delaying or blocking neuronal death until shortly before the onset of degeneration, suggesting a need for altered pattern of protein expression within the cell before death can occur.
In order to identify the antineurotrophic factor originating in the pterothoracic ganglion, aqueous pterothoracic ganglia extracts (PTE) were prepared. SDS-PAGE gels revealed that the size of possible killer-protein may be around 18-20 kilodalton. This antineurotrophic protein is referred to as Manduca "neurocidin". (Abstract shortened by UMI.)
|Rights Information:||Copyright 1993 Choi, Mikyung Kim|
|Date Available in IDEALS:||2011-05-07|
|Identifier in Online Catalog:||AAI9411589|
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