Effects of Different Potassium Ion Concentrations and of Procaine and Pentobarbital on [14C]Glutamate Fluxes in Rat Brain-Cortex Slices

1974 ◽  
Vol 2 (2) ◽  
pp. 274-277 ◽  
Author(s):  
GEORGE B. WEISS ◽  
LEIF HERTZ
Keyword(s):  
Rat Brain ◽  
Brain Cortex ◽  
Potassium Ion ◽  
Ion Concentrations ◽  
Rat Brain Cortex ◽  
Brain Cortex Slices ◽  
Cortex Slices

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.

scholarly journals Effect of triperidol on carbohydrate and amino acid metabolism in rat brain-cortex slices

1968 ◽  
Vol 110 (2) ◽  
pp. 237-241 ◽  
Author(s):  
H. Michalek ◽  
G. L. Gatti ◽  
F. Pocchiari
Keyword(s):  
Rat Brain ◽  
Amino Acid Metabolism ◽  
Brain Cortex ◽  
Acid Metabolism ◽  
Appreciable Effect ◽  
Metabolic Pattern ◽  
Rat Brain Cortex ◽  
14Co2 Production ◽  
Brain Cortex Slices ◽  
Cortex Slices

1. The effect of triperidol on the metabolism of glucose, pyruvate, glutamate, aspartate and glycine was studied with rat brain-cortex slices, U−14C-labelled substrates and a quantitative radiochromatographic technique. 2. Triperidol at a concentration of 0·2mm decreased the oxygen uptake and the 14CO2 production by about 30% when glucose, pyruvate and glutamate were used as substrates, whereas no effects were observed with aspartate and glycine. 3. The drug did not alter qualitatively the metabolic pattern of the substrates. 4. Quantitatively, triperidol decreased the incorporation of 14C from [U−14C]glucose and [U14-C]-pyruvate into glutamate, glutamine and γ-aminobutyrate but not into lactate, alanine and aspartate. The overall utilization rates of glucose and pyruvate were decreased. The relative specific radioactivities of glutamate and aspartate were also decreased. 5. Triperidol increased the rate of disappearance of U−14C-labelled glutamate, aspartate and glycine from the incubation medium, and altered the distribution of their metabolites between medium and tissue. 6. No appreciable effect of triperidol on [1−14C]galactose disappearance was found.

THE EFFECTS OF ALIPHATIC ALDEHYDES ON THE RESPIRATION OF RAT BRAIN CORTEX SLICES AND RAT BRAIN MITOCHONDRIA

1958 ◽  
Vol 36 (6) ◽  
pp. 531-541 ◽  
Author(s):  
C. T. Beer ◽  
J. H. Quastel
Keyword(s):  
Rat Brain ◽  
Mitochondrial Respiration ◽  
Brain Cortex ◽  
Brain Mitochondria ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Rat Brain Cortex ◽  
Low Concentrations ◽  
Brain Cortex Slices ◽  
Cortex Slices

A study has been made of the effects of acetaldehyde and n-valeric aldehyde on the respiration of rat brain cortex slices in the presence and absence of 0.1 M KCl. Acetaldehyde at low concentrations (1–2 mM) brings about a marked inhibition of potassium-stimulated respiration of brain cortex slices. The inhibition by acetaldehyde occurs at 1/200th the concentration at which ethanol produces the same effects. The stimulation of brain respiration due to potassium ions is abolished by acetaldehyde at concentrations that have no observable effect on the unstimulated respiration. Acetaldehyde and n-valeric aldehyde, at equivalent concentrations, have almost equal inhibitory effects on potassium-stimulated rat brain cortex respiration. The inhibitory effects of the aldehydes do not increase sharply with increase of their concentrations, in contrast to the effects of the corresponding alcohols. The aldehydes, in contrast to the corresponding alcohols, inhibit brain mitochondrial respiration as markedly as they inhibit brain cortex respiration. The inhibitory effect of the aldehyde on mitochondrial respiration with pyruvate as substrate is greater in the presence of small quantities of malate than in the absence of malate. The acetaldehyde inhibition is abolished on the addition of DPN. The results obtained with the aldehydes do not support the view that the corresponding alcohols exercise their inhibitive effects on brain respiration by preliminary conversion to the aldehydes. It is suggested that the aldehydes exercise their inhibitory effects on brain respiration by rapid attainment of equilibrium with a constituent of the brain respiratory system associated with a rate-limiting step in the citric acid cycle.

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