Efflux of Phenylalanine From Rat Cerebral Cortex Slices as Influenced by Extra‐ and Intracellular Amino Acids

Korpi, Esa R.; Oja, Simo S.

doi:10.1111/j.1471-4159.1979.tb04562.x

Cited by 41 publications

(14 citation statements)

References 24 publications

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“…Toth and Lajtha (1977) have described a similar acceleration in transport from blood to brain by previous injections of unlabeled amino acids into the cerebral ventricles of mice, and Korpi and Oja (1979), an acceleration from rat brain slices into the medium. It must be emphasized that this effect has no physiological significance, since it is reflected only in an acceleration of isotopic movement, and may be likened to the exchange diffusion of Ussing (1947).…”

Section: Substrate-facilitated Transportmentioning

confidence: 89%

Ventriculo–cisternal perfusion of twelve amino acids in the rabbit

et al. 1982

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The clearances of twelve amino acids from the ventricles during ventriculo-cisternal perfusion in the rabbit have been measured; uptake by the brain was also measured and this permitted the separate computation of loss to brain and loss to blood during the perfusion. Clearance under carrier-free conditions was greater than when a concentration of 5mM unlabeled amino acid was present in the perfusion fluid. Brain uptake was also usually reduced by the presence of unlabeled amino acid due presumably to suppression of accumulation by brain cells. Reduction of transport across the blood-brain barrier would tend to increase brain uptake, and there was some evidence for a balance between the two opposing tendencies. Inhibition of clearance of a given labeled amino acid could be brought about by unlabeled amino acids of different molecular species. In general, the amino acids fell into three categories: neutral, acidic, and basic, and there was some overlap between them; of the neutral amino acids the A- and L-classification of Christensen was valid, although once again there was some overlap. If, during ventriculo-cisternal perfusion of a labeled amino acid, the activity of this labeled amino acid in the blood was raised well above that in the inflowing perfusion fluid, the labeled amino acid continued to be cleared from the perfusion fluid, suggesting uphill transport. On this basis it was suggested that the normally low concentrations of amino acids in the cerebrospinal fluid (CSF), by comparison with those in plasma, were due to an active transport from the CSF to the blood. Substrate-facilitated transport, whereby the penetration of labeled amino acid into the perfusion fluid from blood could be accelerated by adding unlabeled amino acid to the perfusion fluid, or vice versa, was demonstrated.

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Section: Substrate-facilitated Transportmentioning

confidence: 89%

Ventriculo–cisternal perfusion of twelve amino acids in the rabbit

et al. 1982

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“…Cerebral cortex slices 0.5 mm thick prepared from adult male NMRI mice were preincubated and superfused the efflux rate constants (kl, k2, and k3) for GABA and taurine were computed as negative slopes for linear regression lines fitted to the logarithm of the permillage of the remaining radioactivity in the slices vs. superfusion time [Korpi and Oja, 1979;Figs. 1, 21.…”

Section: Methodsmentioning

confidence: 99%

Cation effects on taurine release from brain slices: Comparison to GABA

Oja

Kontro

1987

J of Neuroscience Research

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The effects of cations on the spontaneous and potassium-stimulated taurine release from mouse cerebral cortex slices were assessed with an emphasis on the as yet unestablished calcium dependence of the stimulated release. Spontaneous and stimulated GABA release was analyzed for comparison. A depolarizing concentration (50 mM) of potassium ions caused an approximately 3.5-fold increase in taurine release and the omission of sodium a 6-fold enhancement. GABA release was increased by the same stimuli about 20- and 34-fold, respectively. Omission of calcium ions greatly enhanced basal taurine and GABA release when the medium was supplemented with the calcium chelator ethylenediaminetetraacetate. The potassium stimulation was then abolished, however, with taurine even more readily than with GABA. Magnesium and calcium ions had antagonistic effects on the stimulated release, more clearly with taurine than with GABA. Verapamil abolished the potassium stimulation of both taurine and GABA release, the latter being more sensitive. Although the stimulated taurine release was less in magnitude and had a slower time course than the GABA release, the results are not at variance with the possible neurotransmitter role of taurine.

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“…The efflux rate constants of taurine for the time intervals of 20-30 min (k1) and 34-50 min (k2) were computed as negative slopes of the linear regression lines fitted to the logarithm of the radioactivity remaining in the slices vs superfusion time (Korpi and Oja, 1979). The constants k2 are given as percentages of the corresponding k, values for each slice in order to minimize interexperimental variation.…”

Section: Taurine Release In T-induced He In Rats 27mentioning

confidence: 99%

Taurine release from brain slices in thioacetamide-induced hepatic encephalopathy in rats

Wysmyk

Oja

Saransaari

1991

Molecular and Chemical Neuropathology

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The possible involvement of taurine in the pathogenesis of hepatic encephalopathy was studied in rats injected with thioacetamide. Spontaneous release of exogenous labeled taurine was not affected in any brain area studied, but the potassium-stimulated release was enhanced in the striatum in thioacetamide-treated rats. High concentrations of ammonium ions also evoked greater release of taurine from striatal slices in rats with thioacetamide-induced hepatic encephalopathy.

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Efflux of Phenylalanine From Rat Cerebral Cortex Slices as Influenced by Extra‐ and Intracellular Amino Acids

Cited by 41 publications

References 24 publications

Ventriculo–cisternal perfusion of twelve amino acids in the rabbit

Ventriculo–cisternal perfusion of twelve amino acids in the rabbit

Cation effects on taurine release from brain slices: Comparison to GABA

Taurine release from brain slices in thioacetamide-induced hepatic encephalopathy in rats

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