scholarly journals Uptake and release of glutamate in cerebral-cortex slices from the rat

1972 ◽  
Vol 128 (5) ◽  
pp. 1117-1124 ◽  
Author(s):  
K. Okamoto ◽  
J. H. Quastel

1. Cerebral-cortex slices from rat brain, loaded with labelled l-glutamate as a result of aerobic incubation with labelled glucose, lost less than 15% of this glutamate on subsequent incubation in the presence of unlabelled glucose and l-glutamate. This indicates that very little exchange occurs between extracellular l-glutamate and glutamate accumulated in the neurons as a result of glucose metabolism. 2. Slices, loaded with labelled l-glutamate as a result of aerobic incubation in a medium containing unlabelled glucose and labelled l-glutamate, lost more than half of this glutamate on subsequent incubation in the presence of unlabelled l-glutamate. This indicates that exchange occurs between extracellular glutamate and glutamate accumulated in brain slices as a result of its uptake from the incubation medium. 3. Evidence was obtained suggesting that only a part of the glutamate, accumulated in brain slices as a result of its uptake from an incubation medium containing both glucose and l-glutamate, entered the neurons; apparently almost all the rest entered the glia. 4. It is concluded that the slices contain a pool of glutamate, derived from glucose and located in the neurons, which is poorly exchangeable with extracellular glutamate, and another pool of glutamate, derived from extracellular glutamate and located in the glia, which is freely exchangeable with extracellular glutamate.

1976 ◽  
Vol 26 (5) ◽  
pp. 1007-1014 ◽  
Author(s):  
L. P. Davies ◽  
G. A. R. Johnston

1980 ◽  
Vol 190 (2) ◽  
pp. 333-339 ◽  
Author(s):  
M C W Minchin

1. Protoveratrine A increased the release of gamma-amino[3H]butyrate from small slices of rat cerebral cortex. This effect increased with increasing protoveratrine concentration, reaching a maximum at 100 microM. 2. Removal of Ca2+ from the superfusing medium did not change the increase in release due to 10 microM-protoveratrine; however, the Ca2+ antagonists, compound D-600, La3+, Mn2+, Mg2+ and also high Ca2+ concentration inhibited the effect of the alkaloid, as did procaine. 3. Protoveratrine A increased the uptake of 22Na+ into the slices with a similar dose-response curve to that found for gamma-aminobutyrate release. For the most part, the substances that inhibited protoveratrine-stimulated gamma-aminobutyrate release also inhibited 22Na+ uptake, although the correlation was not perfect. 4. Although extracellular Ca2+ is not required for protoveratrine-induced gamma-aminobutyrate release, an increase in Na+ influx that is susceptible to inhibition by some Ca2+ antagonists does appear to be associated with this phenomenon. However, the possibility remains that changes in the free intracellular Ca2+ concentration may be important for transmitter release induced by depolarizing veratrum alkaloids.


1977 ◽  
Vol 55 (3) ◽  
pp. 356-362 ◽  
Author(s):  
A. M. Benjamin ◽  
J. H. Quastel

Acetylcholine, in presence of eserine, has little or no effect on the potassium-ion-suppressed concentrative uptakes of GABA and taurine by rat brain cortex slices in contrast with its effect on those of L-glutamate, L-aspartate, and glycine. Potassium ions at a concentration of 30 μequiv./ml in the incubation medium has a marked suppressive effect on the uptakes of GABA and taurine when there is no apparent change in the sodium ion content of the brain tissue. It is concluded that some factor, besides the change in sodium gradient, operates in the mechanism of potassium suppression of GABA and taurine uptakes. Acetylcholine diminishes the potassium-evoked release of endogenous GABA and taurine from brain slices. Its action is Ca2+ dependent and is diminished by atropine. Acetylcholine does not affect the potassium-accelerated release of GABA from brain slices previously loaded with this amino acid. The differences in uptake and release phenomena exhibited by GABA and taurine from those of L-glutamate and L-aspartate may be due to differences between the mechanisms, as well as the sites, of cerebral uptake and release of these two groups of amino acids.


1962 ◽  
Vol 40 (1) ◽  
pp. 1439-1448
Author(s):  
J. P. von Wartburg

Rat brain cortex slices were incubated with 5-hydroxytryptophan-3-C14. A method for determination of 5-hydroxytryptamine-C14 and 5-hydroxyindolacetic acid-C14 formed in brain slices is described. Effects of inhibitors of 5-hydroxytryptophan decarboxylase and monoamine oxidase on the metabolic pathway of 5-hydroxytryptophan-3-C14 were measured. α-Methyl dopa (0.33 mM) decreased the level of 5-hydroxyindolacetic acid to a greater amount than that of 5-hydroxytryptamine. Iproniazid (3.3 mM) resulted in an accumulation of 5-hydroxytryptamine and a decrease of 5-hydroxyindolacetic acid formation of 65%. Pheniprazine (0.1 mM) exerted an inhibitory effect on both 5-hydroxytryptophan decarboxylase and monoamine oxidase. Chlorpromazine (0.5 mM) decreased the level of 5-hydroxytryptamine 60% and had a synergistic effect with the inhibition on respiration of brain slices and 5-hydroxytryptophan transport exerted by 0.2 M n-propanol.


1981 ◽  
Vol 36 (3) ◽  
pp. 881-885 ◽  
Author(s):  
J. H. Skerritt ◽  
G. A. R. Johnston

2007 ◽  
Vol 114 (9) ◽  
pp. 1155-1159 ◽  
Author(s):  
N. Maruoka ◽  
T. Murata ◽  
N. Omata ◽  
Y. Takashima ◽  
Y. Fujibayashi ◽  
...  

1999 ◽  
Vol 106 (11-12) ◽  
pp. 1075-1087 ◽  
Author(s):  
T. Murata ◽  
N. Omata ◽  
Y. Fujibayashi ◽  
A. Waki ◽  
N. Sadato ◽  
...  

2004 ◽  
Vol 143 (3) ◽  
pp. 388-396 ◽  
Author(s):  
Uwe Christians ◽  
Sven Gottschalk ◽  
Jelena Miljus ◽  
Carsten Hainz ◽  
Leslie Z Benet ◽  
...  

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