Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.795870
Title: Stress induced taurine release in insects and its effect on the central nervous system
Author: Whitton, Peter Stuart
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 1987
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Abstract:
The underlying cause of the increase in taurine concentration in the haemolymph and nervous system of stressed insects, and the effects of taurine on the nervous system, was studied in the locust (Schistocerca americana qreqaria). The results may be summarised as follows. 1. Taurine was present in all tissues of the locust investigated, and was particularly concentrated in the flight muscle and eye. 2. When insects were poisoned with the GABA antagonist picrotoxin, a redistribution of taurine was observed in which the concentration of the amino acid was increased in haemolymph, nervous tissue, and fat body, and fell in flight muscle and eye. There was no gross change in the whole body content of taurine. Flying and insecticide poisoning also increased taurine concentration in the haemolymph. 3. Exogenous 14C-taurine introduced into the haemolymph accumulated in flight muscle, eye and thoracic ganglia and was retained for a considerable period. No metabolism of 14C-taurine by these tissues was observed. Clearance of 14C-taurine from haemolymph was inhibited by low-temperatures and strucural analogues of taurine (hypotaurine, -alanine and GABA), suggesting that this process requires energy and is carrier mediated. 4. Taurine appears to be biosynthesised via two possible pathways in the locust. From cysteine to cysteine sulphinic acid and thereafter via either hypotaurine or cysteic acid to taurine. Taurine biosynthesis is much greater during the first days of adulthood than in fully mature adult locusts. Flying and picrotoxin poisoning both increase taurine biosynthesis in vivo in all locust tissues. 5. 3H-Taurine was not taken up into locust synaptosomes (in contrast to what is seen in mammals), whereas 3H-GABA was readily accumulated. Taurine and nipecotic acid both caused a concentration- dependent decrease in 3H-GABA uptake into synaptosomes. 6. Locust synaptosomes were observed to accumulate 45Ca++ , and this was greatly increased when synaptosomes were depolarised by either veratridine or high K+ concentration. Taurine caused a con- centration-dependent decrease in 45Ca++ uptake into depolarised and resting synaptosomes, but was relatively less effective in the latter case. GABA and leucine did not reduce 45Ca++ uptake into veratridine-depolarised synaptosomes, but verapamil and tetrodo-toxin were both effective in this respect. 7. Taurine was observed to cause a concentration-dependent decrease in 3H-ACh release from locust synaptosomes following veratridine or K+ depolarisation. 8. Taurine was observed to cause a concentration-dependent increase in 3H-GABA release from synaptosomes. Since nipecotic acid had a similar effect it is suggested that this is due to inhibition of 3 3H-GABA reuptake after depolarisation-induced release. 9. Release of both 3ACh and 3H-GABA from synaptosomes was observed to be calcium-dependent, Veratridine-induced release of transmitters was found to be abolished by tetrodotoxin. 10. Mitochondria isolated from flight muscle or thoracic ganglia readily accumulated 45Ca++ , and this was dependent on the external phosphate concentration. In the presence of an inhibitor of mitochondrial calcium uptake (ruthenium red) or a strong calcium chelating agent (EGTA) a Na+-requiring efflux of calcium was ob- served. Taurine had no effect on 45Ca++ uptake into mitochondria, but was observed to decrease Na+ -dependent calcium efflux, and could thereby decrease intracellular free calcium concentration.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.795870  DOI: Not available
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