Abstract
The human disease caused by niacin (vitamin B3) deficiency is pellagra, a disease that at one time filled insane asylums all over the world before the function of niacin was discovered. The recognition of pellagra as an endemic disease in the US dates from Searcy’s report in 1907 (Strandell et al., 1989) describing 88 cases of dementia in the Mount Vernon, Alabama Insane Asylum. Extensive knowledge about the course of pellagra has since been obtained and this disease has been eradicated as a public health problem; however, exact relationships between niacin deficiency and specific lesions in the central nervous system (CNS) remain poorly defined. Other nutritional deficiencies, common among patients in mental hospitals and in those with senility (Gregory, 1955; Hersov, 1955; McIlwain, 1966), undoubtedly contribute to neuronal dysfunction and exacerbate neurological problems associated with niacin deficiency. Mental symptoms associated with niacin deficiency often precede the dermatitis and other effects of this nutritional deficiency, suggesting a special sensitivity of the nervous system. If initial mental disturbances are not remedied by administration of nicotinic acid or tryptophan, from which nicotinic acid is synthesized in vivo, permanent structural changes occur in cerebral tissue.
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References
Adams D. A., Smith S. J., and Thompson S. H. (1980) Ionic currents in molluscan soma. Ann. Rev. Neurosci. 3,141–167.
Axelrod A. E., Spies T. D, and Elvehjam C. A. (1941) The effect of a nicotinic acid deficiency upon the coenzy me I content of the human. J. Biol. Chem. 138,667–676.
Badawy A. A.-B,, Morgan C. J., Lane J., Dhaliwal K., and Bradley D. M. (1989) Liver tryptophan pyrrolase. A major determinant of the lower brain 5-hydroxytryptamine concentration in alcohol-preferring C57BL mice. Biochem. J. 264, 597–599.
Bain J. A. and Pollock G. H. (1949) Normal and seizure levels of lactate, pyruvate and acid soluble phosphates in the cerebellum and cerebrum. Proc. Soc. Exp. Biol. Med. NY 71, 495–497.
Balazs R., Machiyama Y., Hammond B. J., Julian T., and Richter D. (1970) The operation of the gamma-aminobutyrate bypath of the tricarboxy-lic acid cycle in brain tissue in vitro. Biochem. J. 116, 445–467.
Bender D. A., Smith W. R. D., and Humm R. P. (1977) Effects of benserazide on tryptophan metabolism in the mouse. Biochem Pharmcol. 26, 1619–1623.
Bielicki L. and Krieglstein J. (1976) Inhibition of glucose phosphorylation in rat brain by thiopental. Naunyn-Schmied. Arch. Pharmacol. 293, 25–29.
Blackwood W., McMenemey W. H., Meyer A., Norman R. M., and Russell D. S. (1963) Greenfield’s Neuropathology. Arnold, London.
Boegman R. J. and Albuquerque E. X. (1980) Axonal transport in rats ren dered paraplegic following a single subarachnoid injection of either batrachotoxin or 6-amino-nicotinamide into the spinal cord. J. Neurobiol. 11, 283–290.
Booth R. F. G. and Clarke J. B. (1978) The control of pyruvate dehydrogenase in isolated brain mitochondria. J. Neurochem. 30, 1003–1008.
Brown O. R. and Seither R. L. (1989) Paraquat inhibits NAD biosynthesis at the quinolinic acid synthetase site. Med. Sci. Res. 17, 819–820.
Brunink H. and Wessels E. J. (1972) The determination of nicotinic acid by fluorometric densitometry. Analyst 97, 258,259.
Bruyn R. P. M. and Stoof J. C. (1990) The quinolinic acid hypothesis in Huntington’s chorea. J. Neurol. Sci. 95,29–38.
Brzoska H.-R. and Adhami H. (1975) Electron microscopic study of the effect of 6-AN on the sciatic nerve in newborn rats. Acta Neuropathol. 33 59–6
Buell M. V., Lowry O. R, Roberts N. R., Chang M-L. W., and Kapphahn J. I. (1958) The quantitative histochemistry of the brain. V. Enzymes of glucose metabolism. J. Biol. Chem. 232, 979–993.
Burch H. B., Lowry O. H., Padilla A. M., and Combs A. M. (1956) Effects of riboflavin deficiency and realimentation on flavin enzymes of tissues. J. Biol. Chem. 233, 29–45.
Carpenter K. I. (1981) Effects of different methods of processing maize on its pellagragenic activity. Fed. Proc. 40, 1531–1535.
Chamberlain J. G. and Nelson M. M. (1963) Multiple congenital abnormalities in the rat resulting from acute maternal niacin deficiency during pregnancy. Proc Soc. Exp Biol. Med 112, 836–840.
Chamberlain J. G. (1972) 6-Aminonicotinamide (6AN)-induced abnormali-ties of the developing ependyma and choroid plexus as seen with the scanning electron microscope. Teratology 6, 281–286.
Chui E. and Garcia H. J. (1979) Pathogenesis of 6aminonicotinamide neurotoxicity: New structural analysis, in Progress in Neuropathology, vol.4 (ZimmermanH. M., ed.), Raven Press,New York, pp. 341–359
Churchill L., Dilts R. P., and Kalivas P. W. (1990) Changes in garnmaaminobutyric acid, μ-opioid and neurotensin receptors in the accumbens-pallidal projection after discrete quinolinic acid lesions in the nucleus accumbens. Brain Res. 511, 41–54.
Clark B. R., Halpern R. M., and Smith R. A. (1975) A fluorimetric method for quantitation in the picomole range of N1-methylnicotinamide and nicotinamide in serum. Anal. Biochem. 68, 54–61
Coggeshall R. E. and MacLean P. D. (1958) Hippocampal lesions following administration of 3-acetylpyridine. Proc. Soc. Exp. Biol. Med. 98, 687–689.
Coper H., Hadass H., and Lison H. (1966) Untersuchungen zum mechanismus zentralnervoser funktionsstorungen durch 6-aminonicotinamid. Naunyn-Schmied. Arch. Pharmakol. Exp. Pathol. 255, 96–106.
D’Adamo A. F., Jr. and Haft D. E. (1965) An alternate pathway of alphaketoglutarate catabolism in the isolated, perfused rat liver. I. Studies with DL-glutamate-2-and-5-14C. J Biol. Chem 240, 613–617.
Deguchi T., Ichiyama A., Nishizuka Y., and Hayaishi O. (1968) Studies on the biosynthesis of nicotinamide adenine dinucleotide in the brain. Biochim. Biophys Acta 158, 382–393.
Denson R. (1962) Nicotinamide in the treatment of schizophrenia. Dis Nerv. Syst. 23, 162–172.
Desclin J. C. and Escubi J. (1974) Effects of 3-acetylpyrine on the CNS of the rat, as demonstrated by silver methods. Brain Res. 77,349–364.
Deshpande S. S., Albuquerque E. X., Kauffman F. C., and Guth L. (1978) Physiological, biochemical and histological changes in skeletal muscle, neuromuscular junction and spinal cord of rats rendered paraplegic by subarachnoidal administration of 6-aminonicotinamide. Brain Res. 140, 89–109.
Deutch A. Y., Rosin D. L., Goldstein M., and Roth R. H. (1989) 3-Acetylpyridine-induced degeneration of the nigrostriatal dopamine system: An animal model of olivopontocerebellar atrophy-associated Parkinsonism. Exp. Neural. 105, 1–9.
Dorris R. L. (1989) Interactions of nicotinamide with dopamine receptors in vivo. Pharmacol. Biochem. Behav. 33,915–917.
Dickens F. and Glock G. E. (1951) Direct oxidation of glucose-6-phosphate, 6-phosphogluconate and pentosed-phosphates by enzymes of animal origin. Biochem. J. 50,81–95.
Edstrom J.-E. and Grampp W. (1965) Nervous activity and metabolism of ribonucleic acids in the crustacean stretch receptor neuron. J. Neurochem. 12,735–741.
Fenerty C. A. and Lindup W. E. (1989) Brain uptake of L-tryptophan and diazepam: The role of plasma protein binding. J Neurochem. 53, 416–422.
Frieda R. L. and Bischhausen R. (1978) How do axons control myelin formation? The model of 6-aminonicotinamide neuropathy. J. Neural. Sci. 35, 341–353.
Gal E. M. (1974) Cerebral tryptophan-2,3-dioxygenase (pyrrolase) and its induction in rat brain, J. Neurochem. 22, 861–863.
Gallent M., Bishop M., and Steele G. (1966) DPN (NAD oxidized form): A preliminary evaluation in chronic schizophrenic patients. Ann. Ther. Res. 8, 542.
Garcia-Bunuel L., McDougal D. B., Jr., Burch H. B., Jones E. M., and Touhill E. (1962) Oxidized and reduced pyridine nucleotide levels and enzyme activities in brain and liver of niacin deficient rats. J. Neurochem. 9, 589–594.
Genazzani E. and Di Carlo R. (1974) Inference of neurologically active drugs with metabolism of RNA in brain, in Central Nervous System. Studies on Metabolic Regulation and Function (Genazzani E. and Herken H., eds.), Springer-Verlag, Berlin pp.217–222.
Gerber G. B. and Demo J. (1970) Metabolism of labelled nicotinamide coenzyme in different organs of mice and rats. Proc. Soc. Exp. Biol. Med. 134,689–693.
Gibson G. E., Glantz S., Duffy T. E., and Blass J. P. (1983) Regional brain glucose utilization and behavior during niacin deficiency. Trans. Am. Soc. Neurochem. 14, 121.
Clock G. E., and McLean P. (1954) Levels of enzymes of the direct oxidative pathway of carbohydrate metabolism in mammalian tissues and tumours. Biochem J. 56, 171–175.
Goldsmith G. A. (1958) Niacin-tryptophan relationships in man and niacin requirement. Am. J. Clin. Nutr. 6, 479–486.
Grant W. M. (1980) The peripheral visual system as a target, in Experimental and Clinical Neurotoxicology (Spencer P. S. and Schaumburg H. H., eds.), Williams and Wilkins, Baltimore, pp.77–91.
Gregory I. (1955) The role of nicotinic acid (niacin) in mental health and disease. J. Merit. Sci. 101,85–109.
Griffiths I. R., Kelly P. A. T., and Grome J. J. (1981) Glucose utilization in the CNS in the acute gliopathy due to 6-aminomcotinamide. Lab. Invest. 44, 547–552.
Harkonen M. A. and Kauffman F. C. (1974) Metabolic alterations in the axotomized superior cervical ganglion of the rat. II. The pentose phosphate pathway. Brain Res. 65, 141–157.
Hayes W. J., Jr. (1982) Pesticides Studied in Man. Williams and Wilkins, Baltimore
Heald P. J. (1956) Effects of electrical pulses on the distribution of radioactive phosphate in cerebral tissue. Biochem. J. 63,242–249.
Herken H., Lange K., and Kolbe H. (1969) Brain disorders induced by pharmacological blockade of the pentose phosphate pathway. Biochem. Biophys. Res. Commun. 36, 93–100.
Herken H. (1970) Antimetabolic action of 6aminonicotinamide on the pentose phosphate pathway in the brain, in A Symposium on Mechanisms of Toxicity (Aldridge W. N., ed.), MacMillan, London, pp. 189–203.
Herken H., Lange K., Kolbe H., and Keller K. (1974) Antimetabolic action of the pentose phosphate pathway in the entral nervous sytem induced by 6-aminonicotinamide, in Central Nervous System. Studies on Metabolic Regulation and Function (Genazzani E, and Herken H., eds.), Springer-Verlag, Berlin, pp. 41–54.
Herken H., Meyer-Estorf G., Halbhubner K., and Loos D. (1976) Spastic paresis after 6-aminonicotinamide: Metabolic disorders in the spinal cord and electromyographically recorded changes in the hind limbs of rats. Naunyn-Schmied. Arch. Pharmacol. 293, 245–255.
Hermann A. and Gorman A. L. F. (1981) Effects of 4-aminopyridine on potassium currents in a molluscan neuron. J. Gen. Physiol. 78, 63–86.
Hersov L. A. (1955) A case of childhood pellagra with psychosis. J. Ment. Sci. 101, 878–883.
Heyes M. P., Rubinow D., Lane G, and Markey S. P. (1989a) Cerebrospinal fluid quinolinic acid concentrations are increased in acquired immune deficiency syndrome. Ann. Neural. 26, 275–277.
Heyes M. P., Quearry B. J., and Markey S. P. (1989b) Systemic endotoxin increases L-tryptophan, 5-hydroxyindoleacetic acid, 3 hydroxykynurenine and quinolinic acid content of mouse cerebral cortex. Brain Res. 49l, 173–179.
Hicks S. P. (1955) Pathological effects of antimetabolites. I. Acute lesions in the hypothalamus, peripheral ganglia, and adrenal medulla caused by 3-acetylpyridine and prevented by nicotinamide. Am. J. Pathol. 31, 189–199.
Himwich H. E. (1951) Brain Metabolism and Cerebral Disorders. Williams and Wilkins, Baltimore, MD.
Hoffer A. (1962) Niacin Therapy in Psychiatry. Charles C. Thomas, Springfield, IL
Hoffer A. (1966) The effect of nicotinic acid on the frequency and duration of rehospitalization of schizophrenic patients, a controlled comparison study. Int. J. Neuropsychtr. 2, 234–240.
Horita N., Ishii T., and Izumiyama Y. (1981) Ultrastructure of 6-aminonicotinamide (6-AN)-induced lesions in the CNS of rats. III. Alterations of the spinal gray matter lesions with aging. Acta Neuropathol. 53, 227–235.
Hothersall J. S., Baquer N. Z., Greenbaum A. L., and McLean P. (1979) Alternative pathways of glucose utilization in brain. Changes in the pattern of glucose utilization in brain during development and the effect of phenazine methosulfate on the integration of metabolic routes. Arch. Biochem. Biophys. 198, 478–492.
Hothersall J. S., Zubairu S., McLean P., and Greenbaum A. L. (1981) Alternative pathways of glucose utilization in brain; Changes in the pattern of glucose utilization in brain resulting from treatment of rats with 6-aminonicotmamide. J. Neurochein. 37, 1484–1496.
Hyden H. and Egyhazi E. (1968) The effect of tranylcypromine on synthesis of macromolecules and enzyme activities in neurons and glia. Natrology 18, 732–736.
Ikeda M., Tsuji H., Nakamura S., Ichiyama A., Nishizuka Y., and Hayaishi O. (1965) Studies on the biosynthesis of nicotinamide adenine dinucle-otide. II. A role of picolinic carboxylase in the biosynthesis of nicoti-namide adenine dinucleotide from tryptophan in mammals. J. Biol. Chem. 240, 1395–1401.
Jacobs J. M., Miller R. H., Whittle A., and Cavanagh J. B. (1979) Studies on the early changes in acute isoniazid neuropathy in the rat. Acta Neuropathol. 47, 85–92.
Jepson J. B. (1972) Hartnup disease, in The Metabolic Basis of lnherited Disease (Stanbury J. B., Wyngaarden J. B., and Frederickson D. S., eds.), McGraw Hill, New York, pp. 1486–1503.
Johnson W. J. and McCall J. D. (1955) 6-Aminonicotinamide, a potent nicotinamide antagonist. Science 122, 834.
Kahana S. E., Lowry O. H., Schulz D. W., Passonneau J. V., and Crawford E. J. (1960) The kinetics of phosphoglucoisomerase. J. Biol. Chem. 235, 2178–2184.
Kaplan N. O., Goldin A., Humphreys S. R., Ciotti M. M., and Stolzenbach F. E. (1956) Pyridine nucleotide synthesis in the mouse. J. Biol. Chem. 219, 287–298.
Kaplan N. O. (1960) Neurochemistry of Nucleotides and Amino Acids (Brady R. O. and Tower D. B., eds.), Wiley, New York, pp. 41–54.
Kauffman F. C. (1972) The quantitative histochemistry of enzymes of the pentose phosphate pathway in the CNS of the rat. J. Neurochem. 19, 1–9.
Kauffman F. C. and Johnson E. C. (1974) Cerebral energy reserves and gly-colysis in neural tissue of 6-aminonicotinamide-treated mice. J. Neurobiol. 5, 379–392.
Keller K., Kolbe H., Herken H., and Lange K. (1976) Glycolysis and glyco-gen metabolism after inhibition of hexose monophosphate pathway in C6-glial cells. Naunyn-Schmied. Arch. Pharmacol. 294, 213–215.
Kline N. S., Barclay G. L., Cole J. O., Esser A. H., Lehmann H., and Wittenborn J. R. (1967) Diphosphopyridine nucleotide (DPN) in the treatment of schizophrenia. J. Am. Med. Assoc. 200, 881–882.
Knoll-Kohler E., Wojnorowicz F., and Sarkander H.-J. (1980) Correlated changes in neuronal cerebral rat brain RNA synthesis and hypo-and hypermotoric disorders induced by 6-aminonicotinamide (6-AN). Exp. Brain Res. 38, 173–179.
Kodicek E., Braude R., Kon S. K., and Mitchell K. G. (1959) The availability to pigs of nicotinic acid in tortilla baked from maize treated with lime-water. Br.J. Nutr. 13, 363–384.
Kohler E., Barrach H-J., and Neubert D. (1970) Inhibition of NADP dependent oxidoreductases by the 6-aminonicotinamide analog of NADP. FEBS Lett. 6, 225–228.
Krehl W. A., Teply L. J., and Elvehjem C. A. (1945) Corn as an etiological factor in the production of nicotinic acid deficiency in the rat. Science 101, 283.
Krehl W. A. (1981) Discovery of the effect of tryptophan on niacin deficiency. Fed. Proc. 40, 1527–1530.
Krieglstein J. and Stock R. (1975) Decreased glycolytic flux rate in the isolated perfused rat brain after pretreatment with 6-aminonicotinamide. Naunyn-Schinied. Arch. Pharmacol. 290, 323–327.
Kuhlman R. E. and Lowry O. H. (1956) Quantitative histochemical changes during the development of the rat cerebral cortex. J. Neurochem. 1, 173–180.
Laatsch R. H. (1962) Glycerol phosphate dehydrogenase activity of developing rat CNS. J. Neurochem. 9, 487–492.
Laguna J. and Carpenter K. J. (1951) Raw versus processed corn in niacin-deficient diets. J. Nutr. 45, 21–28.
Lajtha A. L., Maker H. S., and Clarke D. D. (1981) Metabolism and transport of carbohydrates and amino acids, in Basic Neurology (Siegel G. J., Albers R. W., Agranoff B. W., and Katzman R., eds.), Little, Brown, Boston, MA, pp.41–54.
Lange K., Kolbe H., Keller K., and Herken H. (1970) Der kohlenhydratstof fwechsel des gehims nach blockade des pentose-phosphat-weges durch 6-aminonicotinsaureamid. Hoppe-Seyler’s Z. Physiol. Chein. 351, 1241–1252.
Lapin I. P. (1978) Stimulant and convulsive effects of kynurenines injected into brain ventricules in mice. J. Neural Transm. 42, 37–43.
Llinas R., Walton K., Hillman D. E., and Sotelo C. (1975) Inferior olive: Its role in motor learning. Science 190, 1230,1231.
Llinas R., Walton K., and Bohr V. (1976) Synaptic transmission in squid giant synapse after potassium conductance blockage with external 3-and 4-aminopyridine. Biophys. J. 16, 83–86.
Lowry O. H. and Passonneau J. V. (1964) The relationships between substrates and enzymes of glycolysis in brain. J. Biol. Chem. 239, 31–42.
Luine V. N., and Kauffman F. C. (1971) Triphosphopyridine nucleotidede-pendent enzymes in the developing spinal cord of the rabbit. J. Neurochem. l8, 1113–1124.
Madsen J., Abraham S., and Chaikoff I. L. (1964) The conversion of glutamate carbon to fatty acid carbon via citrate. I. The influence of glucose in lactating rat mammary gland slices. J. Biol. Chem. 239, 1305–1309.
McCandless D. W. and Scott W. J. (1981) The effect of 6-aminonicotinamide on energy metabolism in rat embryo neural tube. Teratology 23, 391–395.
McDougal D. B., Jr., Schultz D. W., Passonneau J. V., Clark J. R., Reynolds M. A., and Lowry O. H. (1961) Quantitative studies of white matter. I. Enzymes involved in glucose-6-phosphate metabolism. J. Gen. Physiol. 44, 487–498.
McIlwain H. and Rodnight R. (1949) Breakdown of cozymase by a system from nervous tissue. Biochem. J. 44, 470–477.
McIlwain H. (1966) Biochemistry and the CNS. J & A Churchill, London, pp. 102–126.
Meyer-Estorf G., Schulze P. E., and Herken H. (1973) Distribution of 3H-labelled 6-aminonicotinamide and accumulation of 6-phosphoglu-conate in the spinal cord. Naunyn-Schmied. Arch. Phrmacol. 276, 235–241.
Meyer-Konig E. (1973) Ultrastruktur der Glia-und Axonschadigung durch 6-Aminonicotinamid (6-AN) am Sehnerv der Ratte. Acta Neuropathol. 26, 115–126.
Mosher L. R. (1970) Nicotinic acid side effects and toxicity: A review. Am. J. Psychiatr. 126, 1290–1296.
Nakamura S., Ikeda M., Tsuji H., Nishizuka Y., and Hayaishi O. (1963) Quinolinate transphosphoribosylase: A mechanism of niacin ribonucle-otide formation from quinolinic acid. Biochem Biophys. Res. Commun. 13, 285–290.
Nemeth A. M. and Dickerman H. (1960) Pyridine nucleotides and diphosphopyridine nucleotidase in developing mammalian tissues. J. Biol. Chem. 235, 1761–1764.
Nisslbaum J. S., Packer D. E., and Bodansky O. (1964) Comparison of the actions of human brain, liver, and heart lactic dehydrogenase variants on nucleotide analogs and on substrate analogs in the absence and in the presence of oxalate and oxamate. J. Biol. Chem. 239, 2830–2834.
Osmond H. and Hoffer A. (1962) Massive niacin treatment of schiiophrenia: Review of a nine year study. Lancet 1, 316–319.
Perkins M. N. and Stone T. W. (1983) Quinolinic acid: Regional variations in neuronal sensitivity. Bruin Res. 259, 172–176.
Pfeiffer C. C. (1981) Extranutrients and mental illness. Biol. Psychiatr. 16, 797–799.
Plaitakis A., Nicklas W. J., and Desnick R. J. (1980) Glutamate dehydrogenase deficiency in three patients with spinocerebellar syndrome. Ann. Neural. 7, 297–303.
Politis M. J. (1989) 6-Aminonicotinamide selectively causes necrosis in reactive astroglia cells in vivo. Preliminary morphological observations. J. Neural. Sci. 92, 71–79.
Prakash M. R. and Baquer N. Z. (1981) Inhibition of gamma-aminobutyric acid transaminase with 6-aminonicotinamide in regions of the rat brain. Biochem. Pharmacol. 30, 663–664.
Salter M., Knowles R. G., and Pogson C. I. (1989) How does displacement of albumin-bound tryptophan cause sustained increases in the free tryptophan concentration in plasma and 5-hydroxytryptamine synthesis in brain? Biochem.J. 262, 365–368.
Samson F. E. Jr., and Dahl N. A. (1957) Cerebral energy requirement of neonatal rats. Am. J. Physiol. 188, 277–280.
Sanberg P. R., Calderon S. F., Giordano M., Tew J. M., and Norman A. B. (1989) The quinolinic acid model of Huntington’s disease: Locomotor abnormalities. Exp. Neural. 105, 45–53.
Sarkander H.-I., Knoll-Kohler E., and Cervos-Navarro J. (1978) Repression of glial RNA transcription during the development of 6-aminonicotinamide (6-AN)-induced acute gliopathy. J. Pharmacol. Exp. Ther. 205, 503–514.
Schneider H. and Cervos-Navarro J. (1974) Acute gliopathy in spinal cord and brain stem induced by 6aminonicotinamide. Acta Neuropthal. 27,11–23.
Schwartz R., Whetsell W. O., Jr., and Mangano R. M. (1983) Quinolinic acid: An endogenous metabolite that produces axon-sparing lesions in rat brain. Science 219, 316–318.
Singal S. A., Sydenstricker V. P., and Littlejohn J. M. (1948) The nicotinic acid content of tissues of rats on corn rations. J. Biol. Chem. 176, 1069–1073.
Speciale C.and Schwarcz R. (1990) Uptake of kynurenine into ratbrain slices. J. Neurochem. 54, 156–163.
Speciale C., Ungerstedt U., and Schwartz R. (1989) Production of extracellular quinolinic acid in the striatum studied by microdialysis in unanesthetized rats. Neurosci. Lett. 104,345–350.
Spector R. and Huntoon S. (1981) No effect of maternal niacin deficiency on niacin metabolism in newborn brain. Neurochem. Res. 6, 475–483.
Spector R. and Kelly P. (1979) Niacin and niacinamide accumulation by rabbit brain slices and choroid plexus in vitro. J. Neurochem. 33, 291–298.
Spector R. and Lorenzo A. V. (1975) Myo-inosital transport in the CNS. Am. J. Physiol. 228, 1510–1518.
Spector R. (1979) Niacin and niacinamide transport in the CNS. In vivo studies. J. Neurochem. 33, 895–904.
Stemberg S. S. and Philips F. S. (1958) 6-Aminonicotinamide and acute degenerative changes in the CNS. Science 127, 644–646.
Stone T. W. and Perkins M. N. (1981) Quinolinic acid: A potent endogenous excitant at amino acid receptors in CNS. Eur. J. Phurmacol. 72, 411,412.
Strandell E., Eizirik D. L., and Sandler S. (1989) Survival and B-cell function of mouse pancreatic islets maintained in culture after concomitant exposure to streptozotocin and nicotmamide. Exp. Clin. Endocrinol. 93, 219–224.
Todd W. P., Carpenter B. K., and Schwartz R. (1989) Preparation of 4-halo-3-hydroxyanthranilates and demonstration of their inhibition of 3-hydroxyanthranilate oxygenase activity in rat and human brain tissue. Prep. Biochem. 19,155–165.
Turski W. A., Gramsbergen J. B. P., Traitler H., and Schwartz R. (1989) Rat brain slices produce and liberate kynurenic acid upon exposure to L-kynurenine. J. Neurochem. 52, 1629–1636.
Unna K. (1939) Studies on the toxicity and pharmacology of nicotinic acid. J. Phamtacol. Exp. Ther. 65, 95–103.
Utter M. F. (1950) Mechanism of inhibition of anaerobic glycolysis of brain by sodium ions. J. Biol. Chem. 185, 499–517.
Vezzani A., Stasi M. A., Wu H. Q., Castiglioni M., Weckermann B., and Samanin R. (1989) Studies on the potential neurotoxic and convulsant effects of increased blood levels of quinolinic acid in rats with altered blood-brain barrier permeability. Exp. Neural. 106, 90–98.
Weil-Malherbe H. and Bone A. D. (1951) Studies on hexokinase. I. The hexokinase activity of rat brain extracts. Biochem. J. 49,339–347.
Willing F., Neuhoff V., and Herken H. (1964) Der Austausch von 3-acetylpyridin gegen nicotinsaureamid in den pyridinnucleotiden verschiedener hirnregionen. Naunyn-Schmied. Arch. Pharmacol. 247, 254–266.
Windmueller H. G. and Kaplan N. O. (1962) Solubilization and purification of diphosphopyridine nucleotidase from pig brain. Biochim. Biophys. Acta 56, 388–391.
Winer A. D. (1960) Fluorescent studies of ox-brain lactic and malic dehy-drogenase. Biochem. J. 76, 5p–6p.
Wolf A. and Cowen D. (1959) Pathological changes in the CNS produced by 6-aminonicotinamide. Bull. N.Y. Acad. Med. 35, 814–817.
Woolley D. W. (1952) A Study of Antimetabolites. Chapman and Hall, London
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Kauffman, F.C. (1992). Animal Models of Niacin-Nicotinamide Deficiency. In: Boulton, A.A., Baker, G.B., Butterworth, R.F. (eds) Animal Models of Neurological Disease, II. Neuromethods, vol 22. Humana Press. https://doi.org/10.1385/0-89603-211-6:259
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