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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 28 (1977), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Gamma-hydroxybutyric acid is a neuroactive compound which has been found to be a normal constituent of mammalian brain. The present report characterized enzymatic activity in brain forming gamma-hydroxybutyrate (GHB) from succinic semialdehyde (SSA). When NADPH served as cofactor, whole brain homogenate was capable of forming nearly 300 nmol GHB/min/g brain when enzyme activity was measured at 37°C. GHB production was significantly less (50%) when NADH was the cofactor. A regional localization of these activities indicated that the cerebellum and septal area contained the highest capacity to form GHB in the presence of NADPH; intermediate to high activity was found in the cortex, medulla, superior colliculus and corpus striatum; low activity was present in the inferior colliculus, thalamus, pons, hippocampus, substantia nigra and hypothalamus. Activity in the presence of NADH was rather evenly distributed with the exceptions of the cerebellum and inferior colliculus, which contained high and low activity respectively. Both NADPH- and NADH-dependent activities were found primarily in the cytosol. Pentobarbital inhibited enzyme activity and enzyme activity was differentiated from lactic dehydrogenase and alcohol dehydrogenase by use of specific inhibitors. In addition, mixed substrate experiments and kinetic analysis provided evidence for the presence of two reversible NADPH-dependent enzymes capable of producing GHB from SSA.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 24 (1975), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —The injection of ethanol in mice produced a transient rise in 5-hydroxyindoleacetic acid (5-HIAA) levels in brain. However, no concomitant changes in serotonin (5-HT) levels were noted. In an attempt to explain the biochemical mechanism by which ethanol produced this effect, uptake of tryptophan by brain, serotonin turnover in brain, and transport of 5-HIAA from brain were investigated. No changes in tryptophan levels or uptake into brain of ethanol-treated mice were noted. Ethanol 3 g/kg was found to decrease serotonin turnover. Ethanol was also demonstrated to inhibit the removal of 5-HIAA from the central nervous system, and was found to be an inhibitor of 5-HIAA uptake by isolated choroid plexus. The inhibition of biogenic acid transport was noted even at sub-hypnotic levels of ethanol.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 22 (1974), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of ethanol on serotonin metabolism in brains of mice was determined both after a single injection and ‘chronic’ administration of ethanol. Behavioral effects were also monitored.‘Chronic’ administration of ethanol by inhalation to mice resulted in an increased susceptibility to Metrazole induced seizures. This susceptibility was evident for 48 h after ‘withdrawal’ of mice from ethanol chambers. No differences in brain 5-HT levels between control and ethanol treated mice were evident during withdrawal. However, a significant elevation in brain 5-HIAA levels was noted during this period. Short lived increases in brain 5-HIAA levels were also noted after a single injection of ethanol. Ethanol treatment produced no significant changes in the activity of brain MAO, aldehyde dehydrogenase, or aldehyde reductase. Other mechanisms for ethanol induced increases in brain 5-HIAA are discussed.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 19 (1972), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— The presence of a nonspecific NADH-linked aldehyde reductase was demonstrated in various regions of bovine brain in vitro. With m-nitrobenzaldehyde as substrate, the rate of NADH oxidation was approximately 4 nmol.min-1.(mg of protein)-1 in the cerebellum, pons and medulla; but somewhat lower rates [2–3 nmol.min-1.(mg of protein)-l] were obtained in the other areas of the brain examined. The enzyme was localized primarily in the soluble, supernatant fraction of rat brain homogenates.The enzyme from the supernatant fluid fraction of bovine brain was purified approximately 350-fold by ammonium sulphate fractionation and chromatography on calcium phosphate-gel, DEAE-cellulose and Sephadex G200 columns. The partially purified enzyme catalysed the reduction of a number of aldehydes, including substituted benzaldehydes and aliphatic aldehydes of intermediate chain lengths. Short chain aliphatic aldehydes, such as acetaldehyde, were not reduced by the enzyme and butyraldehyde was a poor substrate. With m-nitrobenzaldehyde as substrate, NADH was oxidized at an approximately 10-fold faster rate than NADPH. The pH optimum for the enzyme was 6.75 for aldehyde reduction, whereas the rate of oxidation of m-nitrobenzylalcohol was optimal at pH 10.0 with NAD as the co-substrate. Km and K3 values ranged from 10 μM to 10 mM for various aldehydes and from 10 to 30 μM for the cofactors.Oxidation of NADH by the partially purified enzyme was not inhibited by 10m pyrazole or by 1 mM phenobarbital. However, the enzyme activity was inhibited by approximately 60 percent by 1 mM chlorpromazine or by 5 mM 1,10-orthophenanthroline. Our data demonstrate that the enzyme is not only separable from the NADPH-linked aldehyde reductase described previously by TABAKOFF and ERWIN, but also is quite different in substrate specificity and inhibitor sensitivity from the ‘classical’, pyrazole-sensitive, NAD- linked alcohol dehydrogenase (EC 1.1.1.1).
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 192 (1993), S. 311-318 
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 63 (1975), S. 957-966 
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 33 (1977), S. 380-381 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Tranylcypromine produces behavioral excitation while pargyline produces depression. Tranylcypromine increased brain tryptophan which led to an accumulation of tryptamine. The levels of tryptamine after tranylcypromine were found to be 3 times those found after pargyline.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 79 (1983), S. 291-294 
    ISSN: 1432-2072
    Keywords: Alcohol ; Genetics ; Intoxication ; Naltrexone ; Opiate receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of naltrexone on the increase in locomotor activity induced by a low dose (1.35 g/kg IP) of ethanol and on the duration of loss of righting reflex after a high dose (3.5 g/kg) of ethanol were studied in BALB/c, DBA/2, and C57BL/6 mice. Ethanol increased locomotor activity in DBA and BALB mice, but not in C57BL mice. Naltrexone, at a dose of 0.1 mg/kg, antagonized the ethanol-induced increase in locomotion similarly in DBA and BALB mice. The duration of loss of ringting reflex was, however, differentially affected in all three strains by naltrexone. The BALB mice were the most sensitive strain (1 mg/kg naltrexone significantly counteracted ethanol hypnosis), the C57BL mice were intermediate (8 mg/kg naltrexone required to antagonize this effect of ethanol), and the DBA mice were least sensitive (no effect evident even at the highest dose of 8 mg/kg) to naltrexone. Thus, naltrexone could antagonize the behavioral effects of a low and high dose of ethanol, but the three strains, which differ in their behavioral response to ethanol, also were differentially sensitive to the effect of naltrexone in reversing ethanol-induced hypnosis and ethanol-induced changes in locomotor activity.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 31 (1975), S. 414-415 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Zusammenfassung Nachweis, dass Pyrogallol und ähnliche Substanzen eine der mitochondrialen Alkoholdehydrogenasen aus Rattenleber hemmen.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 32 (1976), S. 334-336 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Serotonin per se, rather than its metabolites, was shown to produce hypothermia in mice. This effect was mediated within the CNS and could be attenuated by methysergide.
    Type of Medium: Electronic Resource
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