| Project/Area Number |
60570325
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Okayama University Medical School |
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Principal Investigator |
WATANABE Akiharu Associate Professor, First Department of Internal Medicine, Okayama University Medical School, 医学部, 助教授 (00033390)
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1986: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1985: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Hepatic encephalopathy / Hepatic failure / Cynaptosome / Ammonia metabolism / Neurotransmitter / Amino acid / グルタミナーゼ |
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| Research Abstract |
Brain ammonia contents, excitatory (Glu, Asp) and inhibitory (GABA, Gly) amino acid neurotransmitter contents in the synaptosome and binding of Glu and GABA to the neuronal membranes from three different brain areas (prosencephalon, brain stem and cerebellum) of acute hepatic failure rats were determined. Ammonia contents particularly in the prosencephalon and brain stem were much higher than in the blood. Glu contents in the prosencephalon and GABA in the brain stem decreased, and Gln contents in all the areas increased in hepatic failure. Therefore, Glu/Gln ratio decreased, but no change in Glu/GABA and (Glu + Asp)/(GABA + Gly) ratio was observed. Glutamine decarboxylase activity in the synaptosome was not changed in hepatic failure. The maximum binding number (Bmax) in Glu binding to crude neuronal membranes from the brain stem decreased, but dissociation constant (Kd) of Glu binding and both Kd and Bmax of GABA binding were not significantly altered. These results indicate that amino acid neurotransmitter supply from Gln in the synaptosome was impaired by inhibiting glutaminase activity with ammonium ion.
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