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  • 1
    Electronic Resource
    Electronic Resource
    ATP Deficits and Neuronal Degeneration Induced by 3-Nitropropionic Acid (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 648 (1992), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1992.tb24562.x
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  • 2
    Electronic Resource
    Electronic Resource
    INHIBITION OF GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE IN MAMMALIAN NERVE BY IODOACETIC ACID (1971)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 18 (1971), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Cat sciatic nerves were exposed to iodoacetate for a period of 5–10 min and after washing out the iodoacetate, the enzymes, glyceraldehyde-3-phosphate dehydrogenase (d-glyceraldehyde-3-phosphate: NAD oxidoreductase (phosphorylating); EC 1.2.1.12) and lactate dehydrogenase (l-lactate: NAD oxidoreductase; EC 1.1.1.27) were extracted from the high-speed supernatant fraction of nerve homogenates. Concentrations of iodoacetate as low as 2.5 mm could completely block activity of glyceraldehyde-3-phosphate dehydrogenase but had no effect on lactate dehydrogenase. These findings are in accord with the classical concept shown earlier for muscle that iodoacetate blocks glycolysis by its action on glyceraldehyde-3-phosphate dehydrogenase. A complete block of activity of the enzyme was found after treatment with 2 to 5 mm-iodoacetate for a period of 10 min and such blocks were irreversible for at least 3 h. Glyceraldehyde-3-phosphate dehydrogenase activity was NAD specific, with NADP unable to substitute for NAD. The results are discussed in relation to the effect of iodoacetate in blocking glycolysis and in turn the fast axoplasmic transport of materials in mammalian nerve.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1971.tb00013.x
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  • 3
    Electronic Resource
    Electronic Resource
    RELATION OF ATP AND CREATINE PHOSPHATE TO FAST AXOPLASMIC TRANSPORT IN MAMMALIAN NERVE (1972)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 19 (1972), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —ATP and creatine phosphate (CP) levels in cat sciatic nerve maintained in vitro were measured. Anoxia produced by N2 or NaCN or the uncoupling of phosphorylation with DNP reduced the combined levels of ATP + CP to approximately one-half of control levels within 15 min. These agents also blocked fast axoplasmic transport in vitro within 15 min.A block of glycolysis with iodoacetic acid (IAA) reduced the combined levels of ATP + CP to approximately one half of control levels within 1.5–2 h and exposure of nerve in vitro to IAA caused a block of fast axoplasmic transport within the same interval. The correlation of the time at which block of transport occurred with the fall in the level of high-energy phosphates is consistent with the hypothesis that ATP supplies the energy required by the mechanism underlying fast exoplasmic transport.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1972.tb03819.x
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  • 4
    Electronic Resource
    Electronic Resource
    STUDIES ON THE BIOCHEMICAL BASIS OF DISTAL AXONOPATHIES–I. INHIBITION OF GLYCOLYSIS BY NEUROTOXIC HEXACARBON COMPOUNDS (1979)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 32 (1979), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Neurotoxic hexacarbon compounds 2,5-hexanedione (2,5-HD) and methyl n-butyl ketone (MnBK) inhibit crystalline and endogenous CNS and PNS glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Preincubation of the enzyme with the toxin was necessary for inhibition. The enzyme activity of GAPDH was preserved by the addition of dithiothreitol in the presence of either neurotoxin. By contrast, lactate dehydrogenase (LDH) activity was not inhibited by these neurotoxic chemicals. Neurologically inactive compounds 1,6-hexanediol and acetone failed to inhibit GAPDH. The present data indicate that 2,5-HD and M “BK block energy metabolism by inhibiting glycolysis at the site of GAPDH. These observations may account for the known failure of GAPDH-dependent axonal transport and the axonal degeneration which occurs in hexacarbon neuropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1979.tb04550.x
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  • 5
    Electronic Resource
    Electronic Resource
    THE SYNTHESIS OF MYELIN IN DEVELOPING RAT BRAIN (1977)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 29 (1977), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— —The synthesis of myelin proteins has been studied in the grey and white matter slices of developing rat brain by measuring the incorporation of [3H]lysine and [14C]arginine into polypeptide. The incorporation was sensitive to cycloheximide and puromycin at 1 mM concentration. Developing rat optic nerve slices, free of retinal ganglion cells, were able to synthesize myelin basic and proteolipid proteins, but rat retinal preparation failed to synthesize myelin basic protein. Rabbit retinae were able to synthesize myelin basic and proteolipid proteins. Significant activity of the myelin marker enzyme 2′,3′-cyclic nucleotide-2′-phosphodiesterase has been found in the rabbit retina but not in rat retina. The results presented in this communication suggest that myelin proteins in the rat CNS are synthesized by the oligodendroglial cells and that neurons probably do not participate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1977.tb09625.x
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  • 6
    Electronic Resource
    Electronic Resource
    Vitamin E concentrations in different regions of the spinal cord and sciatic nerve of the rat (1986)
    Springer
    Neurochemical research 11 (1986), S. 1419-1424 
    Details
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Since the spinal cord and peripheral nerves are vulnerable to the effects of vitamin E deficiency, vitamin E concentrations in various discrete regions of these parts of the nervous system of the rat were determined. Furthermore, as acrylamide toxicity and vitamin E deficiency share some neuropathological features, tissue vitamin E concentrations in acrylamide-treated rats were also studied. Male Sprague Dawley rats (200 to 250 g body weight) were fed normal rat chow with or without 0.03% acrylamide in their drinking water. After 24 days, the animals were sacrificed and the tissues assayed for vitamin E by a liquid chromatographic method. Vitamin E concentrations decreased from cerebral cortex to spinal cord with no concentration gradients between different levels of the spinal cord. Sciatic nerve concentration of alpha tocopherol was as high as that of cerebral cortex, and the former also contained measurable amounts of gamma tocopherol. Vitamin E concentrations in the majority of nervous tissue samples remained unchanged with acrylamide treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00966221
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