Doctor of Philosophy / General Summary: 1. The mechanisms involved in the pathogenesis of tick paralysis have been investigated in vivo in paralysed dogs and in vitro using nerve-muscle preparations removed from paralysed mice. 2. Neurologic and electromyographic examination of paralysed dogs indicated that tick paralysis involved a failure of neuromuscular transmission* No abnormality of conduction in the nerve trunk could be demonstrated and it was considered that the lesion was likely to be at or near the neuromuscular junction. 3. Nerve-muscle preparations from affected mice were found to be paralysed when examined in vitro. The paralysis was found to be temperature dependent. Results of these experiments supported the contention that the lesion was near the neuromuscular junction. 4. Neuromuscular transmission was examined in preparations from paralysed mice. No abnormality of nerve conduction could be demonstrated. The release of acetylcholine in response to nerve stimulation was depressed due to a reduction in quantal content rather than quantal size. Lowering the temperature of the preparation partially reversed this effect. These results indicated that tick paralysis is due to an abnormality in the mechanism which couples nerve terminal depolarisation and acetylcholine secretion. 5. There is some indication that crude toxin extracted from partially engorged ticks could affect nerve-muscle preparations incubated in it. 6. Apart from some secondary changes no significant morphological abnormalities could be demonstrated in nerve fibres, muscle fibres or neuromuscular junctions from tick paralysed mice.
| Identifer | oai:union.ndltd.org:ADTP/232770 |
| Date | January 1976 |
| Creators | Cooper, Barry John |
| Publisher | University of Sydney., Department of Veterinary Pathology and Bacteriology |
| Source Sets | Australiasian Digital Theses Program |
| Detected Language | English |
| Rights | The author retains copyright of this thesis., http://www.library.usyd.edu.au/copyright.html |
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