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  • Hepatic encephalopathy  (3)
  • hepatic encephalopathy  (3)
  • 1
    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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    Paper (German National Licenses)
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  • 2
    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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  • 3
    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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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Synaptosomal Uptake of Alpha-Ketoglutarate and Glutamine in Thioacetamide-Induced Hepatic Encephalopathy in Rats (1997)
    Springer
    Metabolic brain disease 12 (1997), S. 281-286 
    Details
    ISSN: 1573-7365
    Keywords: Thioacetamide ; hepatic encephalopathy ; glutamine ; α-ketoglutarate ; uptake ; synaptosomes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The kinetics of uptake of two astroglia-derived glutamate (GLU) precursors, α-ketoglutarate (α-KG) and glutamine (GLN) were determined in synaptosomes derived from rats with acute hepatic encephalopathy (HE) induced with a hepatotoxin, thioacetamide (TAA). TAA treatment increased by 33% Vmax for high affinity, low capacity α-KG uptake, without influencing its Km. The increase of the uptake capacity for α-KG may represent a response of the GLUergic nerve terminals to the decreased cerebral α-KG content, which during HE is associated with depressed activity of pyruvate carboxylase, an enzyme that replenishes α-KG in astrocytes. The result is thus consistent with the notion that HE affects the astroglial control of GLUergic neurotransmission. The Km and Vmax for the low affinity, high capacity GLN uptake was not affected by TAA treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1022374109070
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Aspartate aminotransferase, malate dehydrogenase, and pyruvate carboxylase activities in rat cerebral synaptic and nonsynaptic mitochondria: Effects ofin vitro treatment with ammonia, hyperammonemia and hepatic encephalopathy (1991)
    Springer
    Metabolic brain disease 6 (1991), S. 187-197 
    Details
    ISSN: 1573-7365
    Keywords: hepatic encephalopathy ; hyperammonemia ; ammonium chloride ; malate-aspartate shuttle enzymes ; pyruvate carboxylase ; 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 activity of the two malate-aspartate shuttle enzymes: aspartate aminotransferase (AAT), malate dehydrogenase (MDH), and on the pyruvate carboxylase (PC) activity were examined in synaptic and nonsynaptic mitochondria from rat brain. With regard to the shuttle enzymes the response to ammonium ions in vitro (3mM NH4Cl) was observed in nonsynaptic mitochondria only, and was manifested by a 27% decrease of AAT activity and a 16% decrease of MDH activity. By contrast, both in vivo conditions primarily affected the synaptic mitochondrial enzymes: TAA-induced HE produced a 26% decrease of synaptic mitochondrial AAT and a 50% decrease of synaptic mitochondrial MDH. Hyperammonemia inhibited synaptic mitochondrial AAT by 30% and synaptic mitochondrial MDH by 45%. HE produced no effect at all in nonsynaptic mitochondria while hyperammonemia produced a 30% increase in the AAT activity, but no changes in MDH. All the experimental conditions affected the nonsynaptic mitochondrial PC: ammonium chloride in vitro produced a 20% decrease, TAA-induced HE — a 30% decrease, whereas hyperammonemia inhibited the enzyme by 53%. The PC activity in synaptic mitochondria was very low (about 2% of that measured in nonsynaptic mitochondria), which is consistent with the primarily astrocytic localization of the enzyme.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00996918
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