Hostname: page-component-cd9895bd7-jn8rn Total loading time: 0 Render date: 2024-12-29T08:56:58.193Z Has data issue: false hasContentIssue false

Brain glutamate and γ-aminobutyrate (GABA) metabolism in thiamin-deficient rats

Published online by Cambridge University Press:  09 March 2007

Martyn G. Page
Affiliation:
Department of Biochemistry, University College and Middlesex School of Medicine, University College London, Gower Street, London WClE 6BT,
Victor Ankoma-Sey
Affiliation:
Department of Biochemistry, University College and Middlesex School of Medicine, University College London, Gower Street, London WClE 6BT,
William F. Coulson
Affiliation:
Department of Biochemistry, University College and Middlesex School of Medicine, University College London, Gower Street, London WClE 6BT,
David A. Benders
Affiliation:
Department of Biochemistry, University College and Middlesex School of Medicine, University College London, Gower Street, London WClE 6BT,
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

The brain metabolism of glutamate and γ-aminobutyrate (GABA) was investigated in thiamin-deficient and pair-fed control rats, in order to determine whether the GABA shunt may provide an important alternative to 2-oxo-glutarate dehydrogenase (EC 1.2.4.2) in energy-yielding metabolism in thiamin deficiency. Brains from thiamin-deficient animals contained less glutamate, 2-oxo-glutarate and GABA than those from control animals. The brain content of ATP was unaffected by thiamin deficiency. After intracerebroventricular injection of [14C]glutamate, the specific radioactivity of GABA in the brains from deficient animals was 45–50% higher than that in controls, suggesting a considerable increase in the metabolic flux through the GABA shunt in thiamin deficiency. Brain GABA showed a marked circumannual variation, with a peak in mid-summer and a minimum value in mid-winter.

Type
Amino Acids and Proteins: Metabolism and Requirements
Copyright
Copyright © The Nutrition Society 1989

References

REFERENCES

Bergmeyer, H. U. & Bernt, E. (1974). α-Keto-glutarate: ultraviolet spectrophotometric determination. In Methods in Enzymatic Analysis, vol. 3, pp. 16241627 [Bergmeyer, H. U., editor]. New York and London: Academic Press.Google Scholar
Brin, M. (1967). Functional evaluation of nutritional status: thiamine. In Newer Methods of Nutritional Biochemistry, pp. 407445 [Albanese, A. A., editor]. New York and London: Academic Press.Google Scholar
Butterworth, R. F. (1983). Amino acid neurotransmitter function in thiamine deficiency encephalopathy. Journal of Neurochemistry 41, Suppl. S31/D.Google Scholar
Collins, R. C., Kirkpatrick, J. B. & McDougal, D. B. (1970). Some regional pathological and metabolic consequences in mouse brain of pyrithiamine-induced thiamine deficiency. Journal of Neuropathology and Experimental Neurology 29, 5769.CrossRefGoogle ScholarPubMed
Dreyfus, P. M. & Hauser, G. (1965). The effect of thiamin deficiency on the pyruvate decarboxylase system of the cns. Biochimica et Biophysica Acta 104, 7884.CrossRefGoogle Scholar
Gibson, G., Ksiezak-Reding, H., Shen, K., Mykytyn, B. & Blass, J. (1984). Correlation of enzymatic, metabolic and behavioural deficits in thiamin deficiency and its reversal. Neurochemical Research 9, 803814.CrossRefGoogle ScholarPubMed
Gubler, C. J., Adams, B. L., Hammond, B., Chuan-Yuan, E., Guo, S. T. I. & Bennion, M. (1974). Effect of thiamin deprivation and thiamin antagonists on the level of aminobutyric acid and on 2-oxo-glutarate metabolism in rat brain. Journal of Neurochemistry 22, 831836.CrossRefGoogle Scholar
Hamel, E., Butterworth, R. F. & Barbeau, A. (1979). Effect of thiamine deficiency on levels of putative amino acid neurotransmitters in affected regions of rat brain. Journal of Neurochemistry 33, 575577.CrossRefGoogle ScholarPubMed
Hearl, W. & Churchich, J. (1984). Interactions between 4-aminobutyrate aminotransferase and succinic semi-aldehyde dehydrogenase, two mitochondrial enzymes. Journal of Biological Chemistry 259, 1145911463.CrossRefGoogle Scholar
Holowack, J., Kaufmann, F., Ikossi, M. G., Thomas, C. & McDougal, D. B. (1968). The effects of a thiamine antagonist, pyrithiamine, on levels of selected metabolic intermediates and activities of thiamine dependent enzymes in brain and liver. Journal of Neurochemistry 15, 621631.CrossRefGoogle Scholar
Jaworek, D., Gruber, W. & Bergmeyer, H. U. (1974). Adenosine-5-triphosphate: determination with 3-phosphoglyceric acid kinase. In Methods in Enzymatic Analysis, vol. 4, pp. 20972101 [Bergmeyer, H. U., editor]. New York and London: Academic Press.Google Scholar
Kasser, T., Harris, R. & Martin, R. (1985). Levels of satiety: GABA and pentose shunt activities in three brainsites associated with feeding. American Journal of Physiology 248, R453R458.Google ScholarPubMed
Kimura, H. & Kuriyama, K. (1975). Distribution of γ-aminobutyric acid in the rat hypothalamus: functional correlates of GABA with activities of appetite controlling mechanisms. Journal of Neurochemistry 24, 903907.CrossRefGoogle Scholar
McCandless, D. W., Carley, A. D. & Cassidy, C. E. (1976). Thiamine deficiency and the pentose phosphate pathway in rats: intracerebral mechanisms. Journal of Nutrition 106, 11441151.CrossRefGoogle ScholarPubMed
McCandless, D. W. & Schenker, S. (1968). Encephalopathy of thiamine deficiency; studies of intracerebral mechanisms. Journal of Clinical Investigation 47, 22682280.CrossRefGoogle ScholarPubMed
McKhann, G. & Towers, D. (1961). The regulation of γ-aminobutyric acid metabolism in cerebral cortex mitochondria. Journal of Neurochemistry 7, 2632.CrossRefGoogle Scholar
Oser, B. L. (1965). Hawk's Physiological Chemistry, p. 1096. New York: McGraw-Hill.Google Scholar
Parker, W., Hass, R., Stumpf, D., Parks, J., Eguren, L. & Jackson, C. (1984). Brain mitochondrial metabolism in experimental thiamine deficiency. Neurology 34, 14771481.CrossRefGoogle ScholarPubMed
Porter, T. & Martin, D. (1984). Evidence for feedback regulation of glutamate decarboxylase by γ-aminobutyric acid. Journal of Neurochemistry 43, 14641467.CrossRefGoogle ScholarPubMed
Porter, T., Martin, S. & Martin, D. (1986). Activation of glutamate apo-decarboxylase by succinic semi-aldehyde and PMP. Journal of Neurochemistry 47, 468471.CrossRefGoogle Scholar
Rozanov, V. A. (1982). Seasonal changes in the γ-aminobutyric acid system of the mouse brain. Ukrayins'kyi Biokhemichnyi Zhurnal 54, 3640.Google ScholarPubMed
Schousboe, A. (1981). Transport and metabolism of glutamate and GABA in neurons and glial cells. International Review of Neurobiology 22, 145.CrossRefGoogle ScholarPubMed
Udenfriend, S. (1962). Fluorescence Assay in Biology and Medicine, pp. 233236. New York: Academic Press.Google Scholar
van der Heyden, J., de Kloet, E. & Versteeg, D. (1979). GABA content of discrete brain nuclei and spinal cord of the rat. Journal of Neurochemistry 33, 857861.CrossRefGoogle ScholarPubMed
van der Heyden, J. & Korf, J. (1978). Regional levels of GABA in the brain: rapid semi-automated method and prevention of post-mortem increase by 3-mercapto-propionic acid. Journal of Neurochemistry 31, 197203.CrossRefGoogle Scholar
Waynforth, H. B. (1980). Experimental and Surgical Techniques in the Rat, pp. 3436. London: Academic Press.Google Scholar
White, H. L., Howard, J. L., Cooper, B. R., Soroko, F. E., McDermid, J. D., Ingold, K. J. & Maxwell, R. A. (1982). A novel inhibitor of γ-aminobutyrate aminotransferase with anorectic activity. Journal of Neurochemistry 39, 271273.CrossRefGoogle ScholarPubMed
Wirz-Justice, A. (1987). Circadian rhythms in mammalian neurotransmitter receptors. Progress in Neurobiology 29, 219259.CrossRefGoogle ScholarPubMed