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  • 1
    Electronic Resource
    Electronic Resource
    Enhanced Potassium-Stimulated γ-Aminobutyric Acid Release by Astrocytes Derived from Rats with Early Hepatogenic Encephalopathy (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 49 (1987), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Bulk-isolated astrocytes from rats with early hepatogenic encephalopathy (HE) induced with thioacetamide responded to the increase of potassium in the incubation medium from 5 mM to 75 mM with a markedly enhanced release of previously taken up [14C]γ-aminobutyric acid ([14C]GABA). The process was not affected by omission of calcium and/or addition of EGTA to the incubation medium. Only a slight stimulation of GABA release by high potassium was observed in astrocytes from control rats. In contrast, histamine and histidine were vigorously released from control astrocytes in high-potassium medium, and their release was not enhanced by HE, indicating that the observed phenomenon is specific for GABA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1987.tb03385.x
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  • 2
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    Unknown
    Leverkühn oder die Musik als Schicksal (1971)
    Stuttgart, etc. : Periodicals Archive Online (PAO)
    Deutsche Vierteljahrsschrift für Literaturwissenschaft und Geistesgeschichte. 45:2 (1971:Juni) 375 
    Details
    ISSN: 0012-0936
    Topics: German, Dutch and Scandinavian Studies
    URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pao:&rft_dat=xri:pao:article:0088-1971-045-02-000008
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  • 3
    Electronic Resource
    Electronic Resource
    The utility of astroglia cell enriched fraction from rat brain for studying cell membrane potentials: Changes induced by hepatogenic encephalopathy (1985)
    Springer
    Neurochemical research 10 (1985), S. 315-318 
    Details
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00964601
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    The two catalytic components of the 2-oxoglutarate dehydrogenase complex in rat cerebral synaptic and nonsynaptic mitochondria: Comparison of the response to in vitro treatment with ammonia, hyperammonemia, and hepatic encephalopathy (1993)
    Springer
    Neurochemical research 18 (1993), S. 119-123 
    Details
    ISSN: 1573-6903
    Keywords: Hepatic encephalopathy ; hyperammonemia ; ammonium chloride ; 2-oxoglutarate decarboxylase ; lipoamide dehydrogenase ; brain mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of in vitro treatment with ammonium chloride, hepatic encephalopathy (HE) due to thioacetamide (TAA) induced liver failure and chronic hyperammonemia produced by i.p. administration of ammonium acetate on the two components of the multienzyme 2-oxoglutarate dehydrogenase complex (OGDH): 2-oxoglutarate decarboxylase (E1) and lipoamide dehydrogenase (E3), were examined in synaptic and nonsynaptic mitochondria from rat brain. With regard to E1 the response to ammonium ions in vitro (3 mM NH4Cl) was observed in nonsynaptic mitochondria only and was manifested by a 21% decrease of Vmax and a 35% decrease of Km for 2-oxoglutarate (2-OG). By contrast, both in vivo conditions primarily affected the synaptic mitochondrial E1: TAA-induced HE produced an 84% increase of Vmax and a 38% increase of Km for 2-OG. Hyperammonemia elevated Vmax of E1 by 110% and Km for 2-OG by 30%. HE produced no effect at all in nonsynaptic mitochondria while hyperammonemia produced a 35% increase of Vmax and a 30% increase of Km for 2-OG of E1. Both in vivo conditions produced a 20% increase of E3 activity in synaptic mitochondria, but no effect at all in nonsynaptic mitochondria. The preferential sensitivity of E1 to ammonium chloride in vitro in nonsynaptic mitochondria and hyperammonemic conditions in vivo in synaptic mitochondria may play a crucial role in the compartmentation of OGDH responses under analogous conditions. These results confirm the intrinsic differences between the OGDH properties in the synaptic and nonsynaptic brain compartments.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01474673
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  • 5
    Electronic Resource
    Electronic Resource
    Enhanced GABA release in cerebral cortical slices derived from rats with thioacetamide-induced hepatic encephalopathy (1992)
    Springer
    Neurochemical research 17 (1992), S. 1187-1190 
    Details
    ISSN: 1573-6903
    Keywords: Hepatic encephalopathy ; thioacetamide ; cerebral cortex ; GABA release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The release of newly loaded [3H]GABA was studied in slices of different brain regions derived from rats in which acute hepatic encephalopathy (HE) was induced with a hepatotoxin thioacetamide. HE increased both spontaneous and high (50 mM) ammonium chloride-evoked GABA release in cerebral cortical slices by 38% and 50%, respectively. No effects of HE were noted in cerebellar or striatal slices. An increased release of GABA in the cerebral cortex may contribute to the endogenous benzodiazepine-mediated enhancement of GABAergic tone, which is thought to be partly responsible for the pathophysiological mechanism of HE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00968397
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  • 6
    Electronic Resource
    Electronic Resource
    Release of [3H]Dopamine from Striatal and Cerebral Cortical Slices from Rats with Thioacetamide-Induced Hepatic Encephalopathy: Different Responses to Stimulation by Potassium Ions and Agonists of Ionotropic Glutamate Receptors (1997)
    Springer
    Neurochemical research 22 (1997), S. 101-106 
    Details
    ISSN: 1573-6903
    Keywords: Hepatic encephalopathy ; brain slices ; striatum ; frontal cortex ; glutamate receptors ; dopamine release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of depolarizing stimuli; high (50 mM) potassium ions and the glutamate receptor agonists N-methyl-D-aspartate, kainate and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) on the release of newly-loaded [3H]dopamine were studied in frontal cortical and striatal slices from control rats and from rats with acute hepatic encephalopathy induced with a hepatotoxin, thioacetamide. Hepatic encephalopathy enhanced the stimulatory effect of potassium ions by 20% in striatal slices and by 34% in frontal cortical slices. In striatal slices the stimulatory effects of N-methyl-D-aspartate and kainate were depressed in hepatic encephalopathy by 46% and 21%, respectively, which may be taken to reflect impaired modulation of striatal dopamine release by glutamate acting at N-methyl-D-aspartate or kainate receptors. In frontal cortical slices, the stimulatory effect of kainate was enhanced by 35% in hepatic encephalopathy but N-methyl-D-aspartate-stimulated release was not affected. The release evoked by 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate was not affected in hepatic encephalopathy in either brain region. Stimulation of dopamine release in the frontal cortex by depolarization or glutamate acting at kainate receptors could inhibit the activity of descending corticostriatal glutamatergic pathways, further impairing regulation of dopamine release by glutamate in the stratum.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1027347019707
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  • 7
    Electronic Resource
    Electronic Resource
    Some properties of a “crude” fraction of astrocytes prepared with trypsin (1982)
    Springer
    Neurochemical research 7 (1982), S. 519-524 
    Details
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00965503
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  • 8
    Electronic Resource
    Electronic Resource
    The binding of insulin to cerebral capillaries and astrocytes of the rat (1982)
    Springer
    Neurochemical research 7 (1982), S. 489-494 
    Details
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The binding [125I]insulin and its displacement by the unlabeled hormone was measured in vitro in the isolated cerebral capillaries and astroglia cell-enriched fraction as well as in the particulate fraction of cerebral homogenate and liver plasma membrane preparation. The results indicate the specificity and affinity of the hormone binding to astrocytes to be similar to that to cerebral homogenate and liver fractions and markedly higher than to cerebral blood vessels. The possible functional significance of the insulin receptors on astrocytes is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00965500
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  • 9
    Electronic Resource
    Electronic Resource
    Ammonia addedin vitro, but not moderate hyperammonemiain vivo, stimulates glutamate uptake and H+-ATPase activity in synaptic vesicles of the rat brain (1994)
    Springer
    Metabolic brain disease 9 (1994), S. 257-266 
    Details
    ISSN: 1573-7365
    Keywords: hepatic encephalopathy ; hyperammonemia ; ammonium chloride ; ammonium acetate ; synaptic vesicles ; H+-ATPase ; glutamate ; GABA ; dopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The uptake of radiolabelled neurotransmitters: glutamate (GLU), GABA, and dopamine (DA) and the activity of the vacuolar type H+-pumping ATPase (H+-ATPase), were measured in crude synaptic vesicles treatedin vitro with a neurotoxic (3 mM) dose of NH4 + (acetate or chloride), or isolated from rats with a moderate increase of brain ammonia (to ∼ 0.6 mM) induced by i.p. administration of ammonium acetate (HA rats) or a hepatotoxin-thioacetamide (HE rats).In vitro treatment with ammonium salts increased the sodium-independent, chloride-dependent uptake of GLU but did not stimulate the uptake of GABA or DA. Thein vitro treatment also stimulated the H+-ATPase activity. Since H+-ATPase generates the electrochemical gradient driving synaptic vesicular neurotransmitter transport, its stimulation by ammonia may have facilitated GLU uptake. However the GLU specificity of the effect must be related to other factors differentially affecting GLU uptake and the uptake of other neurotransmitters. Enhanced GLU accumulation in the synaptic vesicles may contribute to the increase of synaptic GLU exocytosis previously reported to accompany acute increases of brain ammonia to toxic levels. However, GLU uptake and H+-ATPase activity, but also the uptake of GABA and DA, were unchanged in synaptic vesicles prepared from rats with HA or HE. This indicates that changes in GLU and/or GABA release reported for moderate hyperammonemic conditions must be elicited by factors unrelated to the synaptic vesicular transport of the amino acids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01991199
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  • 10
    Electronic Resource
    Electronic Resource
    Glutamate: A potential mediator of inorganic mercury neurotoxicity (1996)
    Springer
    Metabolic brain disease 11 (1996), S. 175-184 
    Details
    ISSN: 1573-7365
    Keywords: Mercuric chloride ; glutamate neurotoxicity ; astrocytes ; glutamate transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Exposure to mercury vapor (Hgo) produces neurotoxic effects which are for the most part subsequent to its biotransformation in brain to the mercuric cation (Hg2+), which has an exceptionally strong affinity towards the SH groups in proteins. However, neurologic symptoms are often encountered in subjects in which Hg2+ concentration in the brain remains in the submicromolar range, markedly below the anticipated threshold for direct inhibition of cerebral metabolism and function. In this report we review biochemical and morphological evidence obtained in this and other laboratories in tissue culture studies suggesting that in such instances mercury neurotoxicity may be mediated by excitotoxic activity of glutamate (GLU). Mercuric chloride (MC) at 1 μM concentration (or less) inhibits GLU uptake and stimulates GLU release in cultured astrocytes, whichin vivo is likely to result in excessive GLU accumulation in the extracellular space of the CNS. Inhibition of GLU uptake and stimulation of GLU release by MC may be attenuated by addition to the cultures of a cell membrane-penetrating agent dithiothreitol (DTT) but not of glutathione (GSH), which is not transported to the inside of the cells. However, MC-stimulated release of GLU is suppressed when the intracellular GSH levels are increased by metabolic manipulation. The results indicate that the MC-vulnerable SH groups critical for GLU transport are located within the astrocytic membranes. Ultrastructural evidence for GLU-mediated MC neurotoxicity came from studies in an organotypic culture of rat cerebellum. We have shown that: 1) 1 μM MC lowers the threshold of GLU neurotoxicity, 2) the combined neurotoxic effect of GLU plus MC is attenuated by DTT but not by GSH, which is consistent with the involvement of impaired astrocytic GLU transport, and 3) neuronal damage induced by GLU plus MC becomes less accentuated in a medium with dizocilpine (MK-801), a noncompetitive NMDA receptor antagonist.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02069504
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