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.

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.

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.

Inhibition of Rat Brain Protein and Nucleic Acid Synthesis by Cannabinoids In Vitro

1972 ◽  
Vol 50 (6) ◽  
pp. 654-662 ◽  
Author(s):  
Alexander Jakubovič ◽  
Patrick L. McGeer
Keyword(s):  
Nucleic Acid ◽  
Rat Brain ◽  
Brain Cortex ◽  
Weight Fraction ◽  
Adult Rat ◽  
Rat Brain Cortex ◽  
Adult Rat Brain ◽  
Brain Cortex Slices ◽  
Cortex Slices

The effect of Δ9-tetrahydrocannabinol (THC), cannabidiol, and cannabigerol on some metabolic processes in infant and adult rat brain cortex slices was studied in vitro. With L-leucine-U-14C as the tracer substrate, the incorporation of radioactivity into the protein and nucleic acid fractions was significantly inhibited by THC. The oxygen consumption of the slices, the uptake of L-leucine into the slices, and the evolution of 14CO2 were, however, unaffected by THC. Cannabidiol was comparable in activity to THC but cannabigerol was less active. The pattern of inhibition by THC was also observed when the rat brain cortex slices were stimulated by 100 mM K+ or 10 μM protoveratrine. THC also brought about a significant decrease in the incorporation of uridine-2-14C into the nucleic acid fraction of infant and adult rat brain cortex slices. There was a decreased formation of uridine nucleotides in the presence of THC and an increase in uridine and uracil in the low molecular weight fraction. Experiments with THC-2,4-14C established that there was rapid uptake and a concentration of radioactivity in the incubated brain tissue.

Serotonin 5HT1B/1D Receptor Agonists Abolish NMDA Receptor-evoked Enhancement of Nitric Oxide Synthase Activity and cGMP Concentration in Brain Cortex Slices

Cephalalgia ◽  
1999 ◽  
Vol 19 (10) ◽  
pp. 859-865 ◽  
Author(s):  
A Stȩpień ◽  
M Chalimoniuk ◽  
J Strosznajder
Keyword(s):  
Nmda Receptor ◽  
Brain Cortex ◽  
Receptor Agonists ◽  
Adult Rat ◽  
Adult Rat Brain ◽  
Brain Cortex Slices ◽  
Cortex Slices ◽  
The Brain

Our previous studies indicating that the function of excitatory amino acids, NMDA type receptor, is modulated by serotonin focused on the interaction between serotonin 5HT1B/1D and glutamate, NMDA receptor in brain cortex. The effect of agonists of 5HT1B/1D receptor, sumatriptan, and zolmitriptan on NMDA receptor-evoked activation of nitric oxide (NO) and cGMP synthesis in adult rat brain cortex slices was investigated. Two kinds of experiment were carried out using adult rats. In one of them, sumatriptan or zolmitriptan was administered in vivo subcutaneously (s.c.) in a dose of 0.1 mg per kg body weight. Brain slices were then prepared and used in the experiments or, in the other exclusively in vitro studies, both agonists at 10 μM concentration were added directly to the incubation medium containing adult rat brain cortex slices. The data obtained from these studies indicated that stimulation of NMDA receptor in brain cortex slices. The data obtained from these studies indicated that stimulation of NMDA receptor in brain cortex slices leads to a large increase in calcium, calmodulin-dependent NO synthase (NOS) activity and to significant enhancement of the cGMP level. This NMDA receptor-dependent NO and cGMP release was completely blocked by competitive and noncompetitive NMDA receptor antagonists APV (10 μM) or MK-801 (10 μM.), respectively. The specific inhibitor of Ca2+-dependent isoforms of NOS (N-nitro-1-arginine NNLA and 7-nitroindozole (7-N1)) eliminated the NMDA receptor-mediated enhancement of NO and cGMP release. Moreover, the serotonin 5HT1B/1D receptor agonists sumatriptan and zolmitriptan administrated in vivo (s.c.) or in vitro abolished NMDA receptor-evoked NO signalling in brain cortex. The potency of both agonists investigated directly in vitro was similar to their effect after in vivo administration. These results suggest that both serotonin 5HT1B/1D receptor agonists may play an important role in modulating the NO and cGMP-dependent signal transduction pathway in the brain. This effect of sumatriptan and zolmitriptan on NO signaling in the brain system should be taken into consideration when investigating their mechanism of action in the migraine attack.

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.

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