Taurine (2-aminoethane sulfonic acid) is one of the most abundant inhibitory amino acids in the mammalian central nervous system (CNS). Substantial evidence exists to suggest that this amino acid is a physiological modulator of neuronal excitability. Taurine is also a potent anticonvulsant in a variety of animal epilepsies and in certain human epileptics. The mechanisms of these neuromodulatory and anticonvulsant actions of taurine are not known. I have investigated a proposed relationship between altered amino acid metabolism, seizure-susceptibility and the anticonvulsant action of taurine. The findings of the work presented in this dissertation indicate that in the genetically seizure-susceptible rat there are alterations in the subcellular concentration and transport of taurine. Furthermore, the data presented here indicate that these alterations in the CNS handling of taurine are not a consequence of seizure activity but rather may be contributing to the seizure-susceptibility. This supports the hypothesis that taurine is a physiological modulator of neuronal excitability and that defects in this neuromodulatory process may contribute to seizure-susceptibility. The action of taurine was found to not be mediated by a redistribution of glutamate in the brain but instead may be by increasing the conversion of glutamate to GABA.
Identifer | oai:union.ndltd.org:arizona.edu/oai:arizona.openrepository.com:10150/187314 |
Date | January 1983 |
Creators | BONHAUS, DOUGLAS WILLIAM. |
Publisher | The University of Arizona. |
Source Sets | University of Arizona |
Language | English |
Detected Language | English |
Type | text, Dissertation-Reproduction (electronic) |
Rights | Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author. |
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