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  • 1
    Electronic Resource
    Electronic Resource
    Cerebral Cortex Ammonia and Glutamine Metabolism During Liver Insufficiency-Induced Hyperammonemia in the Rat (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 59 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Hyperammonemia has been suggested to induce enhanced cerebral cortex ammonia uptake, subsequent glutamine synthesis and accumulation, and finally net glutamine release into the blood stream, but this has never been confirmed in liver insufficiency models. Therefore, cerebral cortex ammonia- and glutamine-related metabolism was studied during liver insufficiency-induced hyperammonemia by measuring plasma flow and venous-arterial concentration differences of ammonia and amino acids across the cerebral cortex (enabling estimation of net metabolite exchange), 1 day after portacaval shunting and 2, 4, and 6 h after hepatic artery ligation (or in controls). The intra-organ effects were investigated by measuring cerebral cortex tissue ammonia and amino acids 6 h after liver ischemia induction or in controls. Arterial ammonia and glutamine increased in portacaval-shunted rats versus controls, and further increased during liver ischemia. Cerebral cortex net ammonia uptake, observed in portacaval-shunted rats, increased progressively during liver ischemia, but net glutamine release was only observed after 6 h of liver ischemia. Cerebral cortex tissue glutamine, γ-aminobutyric acid, most other amino acids, and ammonia levels were increased during liver ischemia. Glutamate was equally decreased in portacaval-shunted and liver-ischemia rats. The observed net cerebral cortex ammonia uptake, cerebral cortex tissue ammonia and glutamine accumulation, and finally glutamine release into the blood suggest that the rat cerebral cortex initially contributes to net ammonia removal from the blood during liver insufficiency-induced hyperammonemia by augmenting tissue glutamine and ammonia pools, and later by net glutamine release into the blood. The changes in cerebral cortex glutamate and γ-aminobutyric acid could be related to altered ammonia metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb08349.x
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  • 2
    Electronic Resource
    Electronic Resource
    Cerebral Cortex Ammonia and Glutamine Metabolism in Two Rat Models of Chronic Liver Insufficiency-Induced Hyperammonemia: Influence of Pair-Feeding (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 60 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Enhanced cerebral cortex ammonia uptake, subsequent glutamine synthesis, and glutamine release into the bloodstream have been hypothesized to deplete cerebral cortex glutamate pools. We investigated this hypothesis in rats with chronic liver insufficiency-induced hyperammonemia and in pair-fed controls to rule out effects of differences in food intake. Cerebral cortex plasma flow and venous-arterial concentration differences of ammonia and amino acids, as well as cerebral cortex tissue concentrations, were studied 7 and 14 days after surgery in portacaval-shunted/bile duct-ligated, portacaval-shunted, and sham-operated rats, while the latter two were pair-fed to the first group, and in normal unoperated ad libitum-fed control rats. At both time points, arterial ammonia was elevated in the chronic liver insufficiency groups and arterial glutamine was elevated in portacaval shunt/biliary obstruction rats compared to the other groups. In the chronic liver insufficiency groups net cerebral cortex ammonia uptake was observed at both time points and was accompanied by net glutamine release. Also in these groups, cerebral cortex tissue glutamine, many other amino acid, and ammonia levels were elevated. Tissue glutamate levels were decreased to a similar level in all operated groups compared with normal unoperated rats, irrespective of plasma and tissue ammonia and glutamine levels. These results demonstrate that during chronic liver insufficiency-induced hyperammonemia, the rat cerebral cortex enhances net ammonia uptake and glutamine release. However, the decrease in tissue glutamate concentrations in these chronic liver insufficiency models seems to be related primarily to nutritional status and/or surgical trauma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb03253.x
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  • 3
    Electronic Resource
    Electronic Resource
    Specificity of the tryptophan depletion method (1999)
    Springer
    Psychopharmacology 141 (1999), S. 279-286 
    Details
    ISSN: 1432-2072
    Keywords: Key words Tryptophan ; Lysine ; Amino acid ; Mood ; Memory
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Thirteen healthy subjects were subjected to tryptophan (TRP) depletion, lysine (LYS) depletion, and a placebo condition in a double blind cross-over study. The aim of the study was to test the specificity of psychological effects induced by TRP depletion. Subjects ingested a 100 g amino acid mixture with or without TRP or LYS. Six hours later, plasma TRP levels had decreased by 77% in the TRP depletion test and LYS levels by 51% in the LYS depletion condition. After 6 h of TRP depletion, subjects reported significantly more tiredness and lowering of mood, compared to subjects in the placebo group, and memory performance declined. After 6 h of LYS depletion, no significant differences in mood and memory compared to placebo were found. We conclude that the effects of TRP depletion on mood and memory are specific for the depletion of TRP and are not caused by the depletion of an amino acid per se. This supports the hypothesis that TRP depletion affects brain serotonin metabolism and not only brain protein metabolism in general.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050835
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  • 4
    Electronic Resource
    Electronic Resource
    Tryptophan depletion in normal volunteers produces selective impairment in memory consolidation (1999)
    Springer
    Psychopharmacology 141 (1999), S. 362-369 
    Details
    ISSN: 1432-2072
    Keywords: Key words Attention ; Cognition disorders etiology ; Competing amino acids ; Memory disorders chemically induced ; Serotonin biosynthesis ; Serotonergic system ; Tryptophan metabolism ; Verbal learning
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Serotonin (5-hydroxytryptamine; 5-HT) circuits may play a role in cognitive performance, particularly in learning and memory. Cognitive impairment is often seen in depressed patients, in whom 5-HT turnover in the brain is thought to be lowered. A possible human pharmacological model to study the involvement of the serotonergic system in cognitive impairment is to reduce central 5-HT synthesis through L-tryptophan depletion in healthy subjects. In this study, the cognitive effects of tryptophan depletion were assessed and whether genetically or developmentally determined vulnerability factors were predictive of the cognitive impairment induced by tryptophan depletion. Sixteen healthy volunteers with a positive family history of depression and 11 without were given 100 g of an amino acid mixture with or without tryptophan, according to a double-blind, cross-over design. Tryptophan depletion specifically impaired long-term memory performance in all subjects: delayed recall performance, recognition sensitivity, and recognition reaction times were significantly impaired after tryptophan depletion relative to placebo. Short-term memory and perceptual and psychomotor functions were unchanged. There were no differences between groups with a positive and a negative family history for depression. On the basis of these results, it is concluded that tryptophan depletion specifically impairs long-term memory formation, presumably as a result of an acute decrease in 5-HT turnover in the brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050845
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of methionine sulphoximine treatment on renal amino acid and ammonia metabolism in rats (1994)
    Springer
    Pflügers Archiv 427 (1994), S. 524-532 
    Details
    ISSN: 1432-2013
    Keywords: Glutamine synthetase ; Kidney ; Intestine ; Glutamine ; Ammonia ; Amino acids ; Metabolism ; Rat ; In vivo
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Renal glutamine metabolism in relation to ammoniagenesis has been extensively studied during chronic metabolic acidosis, when arterial glutamine levels are reduced. However, little is known about the effects of reduced glutamine delivery on renal glutamine and ammonia metabolism at physiological systemic pH values. Therefore, a model of decreased arterial glutamine concentrations at normal pH values was developed using methionine sulphoximine (MSO). Renal glutamine and ammonia metabolism was measured by determining fluxes and intracellular concentrations after an overnight fast in ether anaesthetized normal rats, MSO-treated rats and their pair-fed controls. Moreover, fluxes and intracellular concentrations of several other amino acids were determined concomitantly. After 2 and 4 days of MSO treatment, arterial glutamine concentrations were reduced to 55%, while arterial ammonia concentrations increased by 70%. Kidney glutamine uptake reduced, but systemic pH was unchanged. Fractional extraction of glutamine remained unchanged, suggesting that also in vivo net uptake of glutamine by the kidney at subnormal levels is related to arterial glutamine concentrations. As a result, at day 2 but not at day 4, the kidney reduced the net release of ammonia into the renal vein and thus reduced net renal ammonia addition to body ammonia pools. Therefore at day 2, the kidney seems to play an important role in adaptation to both hyperammonaemia and hypoglutaminaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374270
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  • 6
    Electronic Resource
    Electronic Resource
    Vascular branching pattern and zonation of gene expression in the mammalian liver. A comparative study in rat, mouse, cynomolgus monkey, and pig (1994)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 239 (1994), S. 441-452 
    Details
    ISSN: 0003-276X
    Keywords: Carbamoylphosphate synthase ; Glutamate dehydrogenase ; Glutamine synthase ; Immunohistology ; In situ hybridization ; mRNA ; Ornithine aminotransferase ; Pericentral ; Periportal ; Phosphoenolpyruvate carboxykinase ; Three-dimensional reconstruction ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Background: A significant part of the liver volume consists of regions in which hepatocytes are in close contact with large branches of the afferent (portal vein) or efferent (hepatic vein) vessels. As most studies have addressed zonation of gene expression around the parenchymal branches of the portal and hepatic vein only, the patterns of gene expression in hepatocytes surrounding larger vessels are largely unknown.Methods: For that reason, we studied the patterns of expression of the mRNAs and proteins of the pericentral marker enzymes glutamine synthase, ornithine aminotransferase, and glutamate dehydrogenase and the periportal marker enzymes phosphoenolpyruvate carboxykinase and carbamoylphosphate synthase in the rat liver, in relation to the branching pattern of the afferent and efferent hepatic veins with immuno and hybridocytochemical techniques. These patterns of expression were compared with those seen in mouse, monkey, and pig liver.Results: The distribution patterns of the genes studied appear to reflect the “intensity” of the pericentral and periportal environment, glutamine synthase and phosphoenolpyruvate carboxykinase requiring the most pronounced environment, respectively. The patterns of gene expression around the large branches of the portal and hepatic vein were found to be related to the parenchymal branches in the neighbourhood of these large blood vessels. Only the cells of the limiting plate retain their periportal and pericentral phenotype for those marker enzymes that do not require a pronounced periportal or pericentral environment to be expressed. GS-negative areas in the pericentral limiting plate appear to correlate with a local absence of draining central veins, and become more frequent and extensive around the larger branches of the hepatic vein.Conclusions: The similarity of the observed patterns of gene expression of the genes studied in mouse, rat, monkey, pig, and man suggests that they reflect a general feature of gene expression in the mammalian liver. A comparison of mouse, rat, pig, and human liver suggests that the presence of glutamine synthase-negative areas reflects the branching order of the efferent hepatic blood vessel. © 1994 Wiley-Liss, Inc.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092390410
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