scholarly journals A Study on the Transamination of Taurine-Glutamic Acid in the Brain

1959 ◽  
Vol 71 (6-1) ◽  
pp. 3107-3109
Author(s):  
Akimasa Imai ◽  
Tatsuo Yamada
Keyword(s):  
Glutamic Acid ◽  
The Brain

scholarly journals Utilization in vivo of glucose and volatile fatty acids by sheep brain for the synthesis of acidic amino acids

1966 ◽  
Vol 101 (3) ◽  
pp. 591-597 ◽  
Author(s):  
R M O'Neal ◽  
R E Koeppe ◽  
E I Williams
Keyword(s):  
Amino Acids ◽  
Fatty Acids ◽  
Glutamic Acid ◽  
Aspartic Acid ◽  
Free Amino Acids ◽  
Free Amino ◽  
Specific Activity ◽  
Tricarboxylic Acid Cycle ◽  
Sheep Brain ◽  
The Brain

1. Free glutamic acid, aspartic acid, glutamic acid from glutamine and, in some instances, the glutamic acid from glutathione and the aspartic acid from N-acetyl-aspartic acid were isolated from the brains of sheep and assayed for radioactivity after intravenous injection of [2-(14)C]glucose, [1-(14)C]acetate, [1-(14)C]butyrate or [2-(14)C]propionate. These brain components were also isolated and analysed from rats that had been given [2-(14)C]propionate. The results indicate that, as in rat brain, glucose is by far the best precursor of the free amino acids of sheep brain. 2. Degradation of the glutamate of brain yielded labelling patterns consistent with the proposal that the major route of pyruvate metabolism in brain is via acetyl-CoA, and that the short-chain fatty acids enter the brain without prior metabolism by other tissue and are metabolized in brain via the tricarboxylic acid cycle. 3. When labelled glucose was used as a precursor, glutamate always had a higher specific activity than glutamine; when labelled fatty acids were used, the reverse was true. These findings add support and complexity to the concept of the metabolic; compartmentation' of the free amino acids of brain. 4. The results from experiments with labelled propionate strongly suggest that brain metabolizes propionate via succinate and that this metabolic route may be a limited but important source of dicarboxylic acids in the brain.

scholarly journals Disruption of Hippocampal Neuregulin 1–ErbB4 Signaling Contributes to the Hippocampus-dependent Cognitive Impairment Induced by Isoflurane in Aged Mice

2014 ◽  
Vol 121 (1) ◽  
pp. 79-88 ◽  
Author(s):  
Xiao-Min Li ◽  
Fan Su ◽  
Mu-Huo Ji ◽  
Guang-Fen Zhang ◽  
Li-Li Qiu ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Acid Decarboxylase ◽  
Neuregulin 1 ◽  
Aged Mice ◽  
Vehicle Injection ◽  
To Receive ◽  
The Brain

Abstract Background: A prolonged isoflurane exposure may lead to cognitive decline in rodents. Neuregulin 1 (NRG1)–ErbB4 signaling plays a key role in the modulation of hippocampal synaptic plasticity through regulating the neurotransmission. The authors hypothesized that hippocampal NRG1–ErbB4 signaling is involved in isoflurane-induced cognitive impairments in aged mice. Methods: Fourteen-month-old C57BL/6 mice were randomized to receive 100% O2 exposure, vehicle injection after 100% O2 exposure, vehicle injection after exposure to isoflurane carried by 100% O2, NRG1-β1 injection after exposure to isoflurane carried by 100% O2, and NRG1-β1 and an ErbB4 inhibitor AG1478 injection after exposure to isoflurane carried by 100% O2. Fear conditioning test was used to assess the cognitive function of mice 48-h postexposure. The brain tissues were harvested 48-h postexposure to determine the levels of NRG1, ErbB4, p-ErbB4, parvalbumin, and glutamic acid decarboxylase 67 in the hippocampus using Western blotting, enzyme-linked immunosorbent assay, and immunofluorescence. Results: The percentage of freezing time to context was decreased from 50.28 ± 11.53% to 30.82 ± 10.00%, and the hippocampal levels of NRG1, p-ErbB4/ErbB4, parvalbumin, and glutamic acid decarboxylase 67 were decreased from 172.79 ± 20.85 ng/g, 69.15 ± 12.20%, 101.68 ± 11.21%, and 104.71 ± 6.85% to 112.92 ± 16.65 ng/g, 42.26 ± 9.71%, 75.89 ± 10.26%, and 73.87 ± 16.89%, respectively, after isoflurane exposure. NRG1-β1 attenuated the isoflurane-induced hippocampus-dependent cognitive impairment and the declines in the hippocampal NRG1, p-ErbB4/ErbB4, parvalbumin, and glutamic acid decarboxylase 67. AG1478 inhibited the rescuing effects of NRG1-β1. Conclusion: Disruption of NRG1–ErbB4 signaling in the parvalbumin-positive interneurons might, at least partially, contribute to the isoflurane-induced hippocampus-dependent cognitive impairment after exposure to isoflurane carried by 100% O2 in aged mice.

EFFECT OF SODIUM GLUTAMATE ON LEUCINE-INDUCED HYPOGLYCEMIA: CLINICAL AND ELECTROENCEPHALOGRAPHIC STUDY

PEDIATRICS ◽  
1961 ◽  
Vol 28 (6) ◽  
pp. 935-942
Author(s):  
Manuel R. Gomez ◽  
James E. Gotham ◽  
John S. Meyer
Keyword(s):  
Glutamic Acid ◽  
Intravenous Administration ◽  
Sodium Glutamate ◽  
Glucose Levels ◽  
Low Glucose ◽  
Electroencephalographic Study ◽  
The Brain

The clinical and electroencephalographic signs of leucine-induced hypoglycemia in the infant can be alleviated with oral or intravenous administration of sodium glutamate. The improvement occurs in spite of low glucose levels in plasma after intravenous administration; this supports the view that glutamic acid is rapidly metabolized by the brain during hypoglycemia.

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