Active Transport of γ-Aminobutyric Acid in Brain Cortex Slices, with Special Reference to Phosphorus-32 Turnover of Phospholipids in Cytoplasmic Particulates

Nature ◽  
1960 ◽  
Vol 186 (4723) ◽  
pp. 474-475 ◽  
Author(s):  
YASUZO TSUKADA ◽  
YUTAKA NAGATA ◽  
SHUSUKE HIRANO
Keyword(s):  
Special Reference ◽  
Active Transport ◽  
Brain Cortex ◽  
Aminobutyric Acid ◽  
Brain Cortex Slices ◽  
Cortex Slices

ACTIVE TRANSPORT OF ASCORBIC ACID IN ADRENAL CORTEX AND BRAIN CORTEX IN VITRO AND THE EFFECTS OF ACTH AND STEROIDS

1963 ◽  
Vol 41 (1) ◽  
pp. 597-604 ◽  
Author(s):  
Shail K. Sharma ◽  
R. M. Johnstone ◽  
J. H. Quastel
Keyword(s):  
Ascorbic Acid ◽  
Adrenal Cortex ◽  
Active Transport ◽  
Brain Cortex ◽  
Acid Uptake ◽  
Dependent Process ◽  
Brain Cortex Slices ◽  
Cortex Slices ◽  
Energy Dependent

Uptake of ascorbic acid-1-C14in brain cortex and adrenal cortex slices is an energy-dependent process. Concentration ratios (i.e. ratios of tissue ascorbic acid-1-C14to medium ascorbic acid-1-C14) greater than 4 have been obtained with both tissues in vitro. Ouabain as well as 2, 4-dinitrophenol suppresses ascorbic acid uptake into brain cortex slices.ACTH inhibits the uptake of ascorbic acid-1-C14in adrenal cortex, but not in brain cortex slices. The presence of glucose is necessary for the inhibition. Several cortical steroids, as well as adenosine-3′,5′-monophosphate, at small concentrations inhibit the uptake. The results are consistent with the interpretation that ACTH inhibits the uptake of ascorbic acid in the adrenal cortex through the steroids produced in its presence.

ACTIVE TRANSPORT OF ASCORBIC ACID IN ADRENAL CORTEX AND BRAIN CORTEX IN VITRO AND THE EFFECTS OF ACTH AND STEROIDS

1963 ◽  
Vol 41 (3) ◽  
pp. 597-604 ◽  
Author(s):  
Shail K. Sharma ◽  
R. M. Johnstone ◽  
J. H. Quastel
Keyword(s):  
Ascorbic Acid ◽  
Adrenal Cortex ◽  
Active Transport ◽  
Brain Cortex ◽  
Acid Uptake ◽  
Dependent Process ◽  
Brain Cortex Slices ◽  
Cortex Slices ◽  
Energy Dependent

Uptake of ascorbic acid-1-C14in brain cortex and adrenal cortex slices is an energy-dependent process. Concentration ratios (i.e. ratios of tissue ascorbic acid-1-C14to medium ascorbic acid-1-C14) greater than 4 have been obtained with both tissues in vitro. Ouabain as well as 2, 4-dinitrophenol suppresses ascorbic acid uptake into brain cortex slices.ACTH inhibits the uptake of ascorbic acid-1-C14in adrenal cortex, but not in brain cortex slices. The presence of glucose is necessary for the inhibition. Several cortical steroids, as well as adenosine-3′,5′-monophosphate, at small concentrations inhibit the uptake. The results are consistent with the interpretation that ACTH inhibits the uptake of ascorbic acid in the adrenal cortex through the steroids produced in its presence.

THE EFFECT OF HYDROXYLAMINE AND AMINOOXYACETIC ACID ON THE CEREBRAL IN VITRO UTILIZATION OF GLUCOSE, FRUCTOSE, GLUTAMIC ACID, AND γ-AMINOBUTYRIC ACID

1965 ◽  
Vol 43 (7) ◽  
pp. 865-876 ◽  
Author(s):  
Bernard Haber
Keyword(s):  
Glutamic Acid ◽  
Aspartic Acid ◽  
Brain Cortex ◽  
Pyridoxal Phosphate ◽  
Aminobutyric Acid ◽  
Aminooxyacetic Acid ◽  
Inhibitory Effects ◽  
Brain Cortex Slices ◽  
Cortex Slices

The aerobic incubation of rat brain cortex slices leads to rapid incorporation of metabolite carbon from both glucose-U-C14 and fructose-U-C14 into glutamic acid, aspartic acid, glutamine, alanine, and γ-aminobutyric acid (γABA). Use of labeled glutamic acid results in a greater incorporation into aspartic acid, and no labeling of alanine. The incorporation from γABA-1-C14 is lowest, and does not result in labeling of alanine. Both hydroxylamine and aminooxyacetic acid (AOAA) abolish the incorporation of metabolite carbon into γABA and alanine, and diminish that of glutamine, with labeling of aspartic acid diminished with fructose as the substrate. Both inhibitors abolish all amino acid labeling from γABA-1-C14, and exert differing effects on incorporation from glutamic acid, depending on the presence or absence of glucose. The respiration of brain cortex slices is markedly diminished by AOAA and by the higher concentration of hydroxylamine, whereas with fructose 0.5 mM hydroxylamine is also effective. Similar inhibitory effects are observed on the C14O2 production. The inhibitory effects of AOAA on incorporation of metabolite carbon from glucose, the respiration, and the carbon dioxide production are reversed by pyridoxal phosphate, and spectrophotometric data indicate that this is due to complex formation between the vitamin and the inhibitor.

BIOCHEMICAL STUDIES ON TOFRANIL

1961 ◽  
Vol 39 (3) ◽  
pp. 551-558 ◽  
Author(s):  
P. N. Abadom ◽  
K. Ahmed ◽  
P. G. Scholefield
Keyword(s):  
Rat Brain ◽  
Rat Liver ◽  
Brain Cortex ◽  
Respiratory Activity ◽  
Liver Mitochondria ◽  
Brain Mitochondria ◽  
Inhibitory Effect ◽  
Rat Liver Mitochondria ◽  
Brain Cortex Slices ◽  
Cortex Slices

Tofranil inhibits the respiratory activity of rat brain cortex slices incubated in a glucose-containing medium. It also inhibits the uptake and incorporation of glycine-1-C14at concentrations which have only a slight inhibitory effect on the respiration of slices. Tofranil also inhibits oxidative phosphorylation in both rat liver and rat brain mitochondria but at higher concentrations respiration is greatly affected. Tofranil differs quantitatively from chlorpromazine in its greater inhibitory effect on the ATP–Pi32exchange reaction and its lesser effect on the cytochrome c oxidase activity of rat liver mitochondria.

EFFECTS OF ACETYLSALICYLATE AND 2,4-DINITROPHENOL ON METABOLISM AND TRANSPORT IN RAT BRAIN CORTEX IN VITRO

1963 ◽  
Vol 41 (2) ◽  
pp. 435-454 ◽  
Author(s):  
O. Gonda ◽  
J. H. Quastel
Keyword(s):  
Amino Acids ◽  
Rat Brain ◽  
Brain Cortex ◽  
Transport Processes ◽  
Rat Brain Cortex ◽  
High K ◽  
Increased Sensitivity ◽  
Brain Cortex Slices ◽  
Cortex Slices

The effects of acetylsalicylate and of 2,4-dinitrophenol on the metabolism and transport processes of rat brain cortex slices incubated at 37° in glucose–Ringer media under various conditions have been investigated. The following processes are suppressed by acetylsalicylate (5 mM) or dinitrophenol (0.05 mM) to a much greater extent in media containing 105 mM KCl or 10 mM NH4Cl (which stimulate brain respiration) than in normal media:(a) respiration;(b) incorporation of phosphate into ATP and ADP;(c) conversion of creatine to phosphocreatine;(d) uptake of glutamate or of creatine from the medium to the tissue.The two drugs increase the leakage of amino acids from rat brain cortex slices into the medium, the effects being greatest in the presence of 105 mM KCl or 5 mM glutamate or in the absence of glucose. They change the yields of labelled amino acids from labelled glucose or labelled glutamate.Labelled glutamate is converted to labelled aspartate, γ-aminobutyrate and glutamine in rat brain cortex slices, the addition of glucose bringing about increased yields of glutamine and γ-aminobutyrate and a decreased yield of aspartate. The formation of labelled glutamine from either labelled glutamate or from labelled glucose is suppressed by acetylsalicylate or dinitrophenol, the effects being greater in the presence of 105 mM KCl or 10 mM NH4Cl.The increased sensitivity of the stimulated tissue metabolism to the drugs, in the presence of high K+, or of NH4+or of glutamate, is probably explained by the fact that there is a fall, under these conditions, in the tissue phosphocreatine level. There is, therefore, less reserve phosphocreatine to maintain the level of ATP when neuronal oxidative phosphorylation is suppressed by the addition of acetylsalicylate or of dinitrophenol.

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