Effects of Lithium Ions in a Pharmacological Concentration on Potassium and Sodium Ions in Rat Brain-Cortex Slices

1973 ◽  
Vol 1 (1) ◽  
pp. 111-114 ◽  
Author(s):  
CHRISTEL S. KJELDSEN ◽  
HENRIK LUND-ANDERSEN ◽  
LEIF HERTZ
Keyword(s):  
Rat Brain ◽  
Brain Cortex ◽  
Sodium Ions ◽  
Lithium Ions ◽  
Rat Brain Cortex ◽  
Brain Cortex Slices ◽  
Cortex Slices

STUDIES OF THE CATIONIC, AND ACETYLCHOLINE, STIMULATION OF PHOSPHATE INCORPORATION INTO PHOSPHOLIPIDS IN RAT BRAIN CORTEX IN VITRO

1963 ◽  
Vol 41 (5) ◽  
pp. 1243-1256 ◽  
Author(s):  
Maurice Brossard ◽  
J. H. Quastel
Keyword(s):  
Rat Brain ◽  
Brain Cortex ◽  
Total Phospholipid ◽  
Sodium Ions ◽  
Inorganic P ◽  
Rat Brain Cortex ◽  
Brain Cortex Slices ◽  
Cortex Slices ◽  
Stimulation Of

The addition of 0.1 M KCl to, or the omission of CaCl2from, incubation media in which rat brain cortex slices are respiring, stimulates the incorporation of inorganic P32into phospholipids. It also stimulates the labelling of 7-minute hydrolyzable nucleotide phosphates, but decreases their levels. The stimulation of P32incorporation into total phospholipid takes place primarily into phosphatidic acid and phosphoinositide but not into phosphatidyl choline and phosphatidyl ethanolamine. The addition of succinate and γ-aminobutyrate to brain cortex slices, metabolizing glucose, markedly inhibits the labelling of phospholipids although the respiration of slices is not diminished. The potassium stimulation of phospholipid labelling only occurs if sodium ions are present in the incubation medium. The lesser stimulation due to absence of calcium ions seems, however, to be independent of the presence of sodium ions. Acetylcholine stimulation of P32incorporation into phospholipids is dependent on the presence of sodium ions. Such stimulations are suppressed by concentrations of malonate, iodoacetate, fluoride, and ethanol that have little effect on the unstimulated incorporation of P32. Atropine and hyoscine inhibit acetylcholine stimulation but not cationic stimulation of P32incorporation. It is suggested that the effect of acetylcholine on P32incorporation is mediated by cationic changes at the nerve cell membrane.

STUDIES OF THE CATIONIC, AND ACETYLCHOLINE, STIMULATION OF PHOSPHATE INCORPORATION INTO PHOSPHOLIPIDS IN RAT BRAIN CORTEX IN VITRO

1963 ◽  
Vol 41 (1) ◽  
pp. 1243-1256 ◽  
Author(s):  
Maurice Brossard ◽  
J. H. Quastel
Keyword(s):  
Rat Brain ◽  
Brain Cortex ◽  
Total Phospholipid ◽  
Sodium Ions ◽  
Inorganic P ◽  
Rat Brain Cortex ◽  
Brain Cortex Slices ◽  
Cortex Slices ◽  
Stimulation Of

The addition of 0.1 M KCl to, or the omission of CaCl2from, incubation media in which rat brain cortex slices are respiring, stimulates the incorporation of inorganic P32into phospholipids. It also stimulates the labelling of 7-minute hydrolyzable nucleotide phosphates, but decreases their levels. The stimulation of P32incorporation into total phospholipid takes place primarily into phosphatidic acid and phosphoinositide but not into phosphatidyl choline and phosphatidyl ethanolamine. The addition of succinate and γ-aminobutyrate to brain cortex slices, metabolizing glucose, markedly inhibits the labelling of phospholipids although the respiration of slices is not diminished. The potassium stimulation of phospholipid labelling only occurs if sodium ions are present in the incubation medium. The lesser stimulation due to absence of calcium ions seems, however, to be independent of the presence of sodium ions. Acetylcholine stimulation of P32incorporation into phospholipids is dependent on the presence of sodium ions. Such stimulations are suppressed by concentrations of malonate, iodoacetate, fluoride, and ethanol that have little effect on the unstimulated incorporation of P32. Atropine and hyoscine inhibit acetylcholine stimulation but not cationic stimulation of P32incorporation. It is suggested that the effect of acetylcholine on P32incorporation is mediated by cationic changes at the nerve cell membrane.

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.

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