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P Kontro

Publications and source records attributed to P Kontro.

At least 37 records · Page 2Linked to original sources
PubMed1987

Cation effects on taurine release from brain slices: comparison to GABA.

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.

Animals↗
PubMed1987

Sodium-dependent high-affinity uptake of taurine in cultured cerebellar granule cells and astrocytes.

Taurine uptake in cultured cerebellar granule cells and astrocytes consisted of a saturable high-affinity component and nonsaturable diffusion. The transport constant (Km) was significantly lower and the maximal velocity (V) higher in granule cells than in astrocytes. The uptakes were strictly sodium dependent and also moderately decreased in potassium-free medium. The specificity profile of taurine uptake was similar in both cell types, hypotaurine, beta-alanine, and guanidinoethanesulphonic acid being the most potent inhibitors, followed by GABA and homotaurine. Glutamate inhibited taurine uptake more in astrocytes than in granule cells. In principle, the uptake systems were similar in granule cells and astrocytes, exhibiting features characteristic of uptake of a neurotransmitter or -modulator.

Animals↗
PubMed1987

Interactions of taurine and dopamine in the striatum.

Both spontaneous and K+-stimulated taurine release from rat striatal slices were affected by dopamine and apomorphine, suggesting that dopaminergic systems are able to modulate taurine release. K+-stimulated dopamine release was potentiated by taurine, which effect may not involve dopamine autoreceptors. Taurine was able to inhibit spiperone binding to striatal membranes in a uncompetitive manner and thus interfere with the function of dopaminergic receptors.

Animals↗
PubMed1987

Taurine and GABA release from mouse cerebral cortex slices: effects of structural analogues and drugs.

The effects of structural analogues, excitatory amino acids and certain drugs on spontaneous and potassium-stimulated exogenous taurine and GABA release were investigated in mouse cerebral cortex slices using a superfusion system. Spontaneous efflux of both amino acids was rather slow but could be enhanced by their uptake inhibitors. Taurine efflux was facilitated by exogenous taurine, hypotaurine, beta-alanine and GABA, whereas GABA, nipecotic acid and homotaurine effectively enhanced GABA release. The stimulatory potency of the analogues closely corresponded to their ability to inhibit taurine and GABA uptake, respectively, indicating that these efflux processes could be mediated by the carriers operating outwards. Glutamate induced GABA release, whereas taurine efflux was potentiated by aspartate, glutamate, cysteate, homocysteate and kainate. The centrally acting drugs, including GABA agonists and antagonists, as well as the proposed taurine antagonist TAG (6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide), had no marked effects on spontaneous taurine and GABA release. Potassium ions stimulated dose-dependently both taurine and GABA release from the slices, the responses of taurine being strikingly slow but sustained. Exogenous GABA and nipecotic acid accelerated the potassium-stimulated GABA release, whereas picrotoxin and bicuculline were ineffective. The potassium-stimulated taurine release was unaltered or suppressed by exogenous taurine and analogues, differing in this respect from GABA release. The apparent magnitude of the depolarization-induced GABA release is thus influenced by the function of membrane transport sites, but the same conclusion cannot be drawn with regard to taurine. Haloperidol and imipramine were able to affect the evoked release of both taurine and GABA.

Animals↗
PubMed1987

Effects of the anticonvulsant taurine derivative, taltrimide, on membrane transport and binding of GABA and taurine in the mouse cerebrum.

The effects of a new anticonvulsive derivative of taurine, taltrimide (2-phthalimido-ethanesulphon-N-isopropylamide), and its metabolites on the release, uptake and binding of gamma-aminobutyric acid (GABA) and taurine, were studied in the cerebrum of the mouse. The potassium-stimulated release of taurine from slices of cerebral cortex was inhibited in vitro by taltrimide and its dealkylated metabolite, whereas the stimulated release of GABA was significantly enhanced by both drugs. The uptake of taurine and GABA were not markedly affected. Both taltrimide and its dealkylated metabolite strongly inhibited the sodium-independent binding of taurine to synaptic membranes of brain, the effects on the binding of GABA being less pronounced. The actions on synaptic binding of taurine and on depolarization-stimulated release of GABA may be of significance for their anticonvulsant properties.

Animals↗
PubMed1987

Co-operativity in sodium-independent taurine binding to brain membranes in the mouse.

Sodium-independent taurine binding to mouse brain membranes treated twice with Triton X-100 exhibited properties of positive co-operativity, suggesting that two or more taurine molecules interact at the binding site. The proposed taurine antagonist 6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide and the new anticonvulsant taurine derivative taltrimide as well as glycine and GABA with their antagonists displaced taurine binding, strychnine being the most effective.

Animals↗
PubMed1987

Glycinergic systems in the brain stem of developing and adult mice: effects of taurine.

The release of glycine from slices of the brain stem and binding of strychnine to brain stem membranes were characterized in adult and developing mice. Spontaneous glycine efflux was markedly facilitated by homoexchange with exogenous glycine and moderately by heteroexchange with taurine. Potassium stimulation released more glycine from brain stem slices from adult than from 7-day-old mice. Potassium-stimulated glycine release was also potentiated by glycine and by the novel anticonvulsant taurine derivatives. One population of strychnine-binding sites was found in both mature and immature brain stem. The number of binding sites increased with age, whereas the affinity of the sites for strychnine remained the same. The glycine inhibition was stronger in adult than in developing mice. In the presence of taurine the affinity for strychnine decreased without any change in the maximal binding capacity, suggesting a competitive type of inhibition. The binding constant and maximal binding capacity of strychnine increased in the presence of NaCl (200 mM) both in adult and 7-day-old mice. The calculated IC50 values for displacement of strychnine binding by glycine, taurine and beta-alanine were higher in the presence than in the absence of sodium. The results show that the evoked release of glycine and the number of binding sites of strychnine increase during postnatal development in the mouse but that their characteristics do not change.

Aging↗
PubMed1987

Taurine and GABA binding in mouse brain: effects of freezing, washing and Triton X-100 treatment on membranes.

The sodium-independent binding of taurine and GABA were determined with mouse brain membranes subjected to various freezing-thawing cycles, washing procedures and Triton X-100 treatments. The treated membranes were characterized by electron microscopy and determination of their content of endogenous free amino acids, e.g., taurine, GABA, glutamate, aspartate and glycine. The washings and the detergent gradually disrupted all synaptic structures, yielding empty-looking sealed membrane pouches of various sizes. Only traces of taurine, GABA, aspartate and glutamate were present in the Triton X-100-treated membranes, whereas these membranes still contained some glycine. Concomitantly, the affinity and maximal capacity of GABA binding increased, indicating that the treatments progressively removed some endogenous GABA binding inhibitors. Saturable taurine binding became detectable only after the Triton X-100 treatment, endogenous taurine, removable from membranes only with difficulty, obviously hampering binding measurements.

Amino Acids↗
PubMed1986

Modulation of the GABA-benzodiazepine receptor complex by taurine in rat brain membranes.

The interactions of taurine and its precursor hypotaurine with the GABA-benzodiazepine receptor complex were studied by investigating their effects on GABA and flunitrazepam binding in rat brain membranes. Taurine, and to a lesser degree also hypotaurine, displaced the high- and low-affinity GABA binding. The maximal binding capacities of both sites were decreased in the presence of taurine, while the binding constants remained the same, suggesting noncompetitive interactions. Taurine and hypotaurine affected flunitrazepam binding only at a very high concentration (50 mmol/l), whereas GABA (within the concentration range of 0.1-100 mumol/l) significantly enhanced the binding. Taurine inhibited the GABA-stimulated binding dose-dependently. These modulatory effects of taurine on the GABA-benzodiazepine receptor complex could result from interactions with the GABA recognition site but not from direct actions on the benzodiazepine site.

Animals↗
PubMed1986

High-affinity uptake of taurine and beta-alanine in primary cultures of rat astrocytes.

The kinetics and specificity of taurine and beta-alanine uptake were studied in primary cultures of rat astrocytes under identical experimental conditions. The uptake consisted of nonsaturable penetration and saturable high-affinity transport that was strictly sodium dependent. The cells accumulated taurine more effectively than beta-alanine, both the affinity and uptake capacity being greater for taurine. Taurine uptake was competitively inhibited by beta-alanine and GABA, the former being more potent. Also, hypotaurine and 2-guanidinoethanesulphonic acid strongly reduced taurine uptake, but L-2,4-diaminobutyric acid had no significant effect. beta-Alanine uptake was also competitively inhibited by GABA, but the most potent inhibitors were hypotaurine and 2-guanidinoethanesulphonic acid. L-2,4-Diaminobutyric acid was moderately active. The uptake systems for taurine and beta-alanine were thus in principle similar, and they exhibited certain characteristics typical for a neurotransmitter amino acid. The inhibition studies further suggest the existence of only one common transport system for taurine, beta-alanine, and GABA in cultured primary astrocytes. The same uptake system may also be used for hypotaurine.

Alanine↗
PubMed1986

Taurine interferes with spiperone binding in the striatum.

The effects of taurine and its structural analogues and two new anticonvulsant derivatives, taltrimide and MY-103, on the function of brain dopaminergic systems were studied by assessing their interference with the binding of [3H]spiperone to synaptic membranes isolated from rat striata. Two populations of binding sites were detected. The binding was effectively displaced by (+)butaclamol and dopamine, serotonin being less potent by one order of magnitude. Taurine, taltrimide and MY-103 inhibited spiperone binding moderately. The binding constants of both high- and low-affinity components and the maximal binding capacity of the low-affinity component decreased in the presence of taurine. The results show that taurine and its novel anticonvulsant derivates could modulate the function of striatal dopaminergic systems.

Animals↗
PubMed1986

Free amino acids of rat astrocytes in primary culture: changes during cell maturation.

The concentrations of free amino acids were analysed in cultured primary astrocytes during cell maturation and in the starting material, i.e. the cerebral hemispheres of newborn rats. Taurine was the most abundant amino acid in all samples, the content of glutamine being comparable only in immature astrocytes (7 days in culture). The intracellular levels of most amino acids significantly decreased during the first 2 weeks in culture, remaining fairly stable during the third week.

Amino Acids↗
PubMed1985

Release of preloaded taurine and hypotaurine from astrocytes in primary culture: stimulation by calcium-free media.

The spontaneous and stimulated release of taurine and hypotaurine from astrocytes in primary cultures were investigated. Spontaneous efflux was slow, less than one half of preloaded labeled taurine and hypotaurine still remaining in the cells after a 60-min efflux period. The release processes of both amino acids were in principle similar. No homo- or heteroexchange with extracellularly added taurine, hypotaurine or GABA could be detected, and depolarizing potassium concentrations failed to stimulate taurine or hypotaurine release. On the other hand, omission of calcium ions from medium increased efflux of taurine and hypotaurine about three- and twofold, respectively, in both high-K+ and normal-K+ media.

Animals↗
PubMed1985

Mechanisms of stimulated taurine release from nervous tissue.

Spontaneous taurine efflux from brain cells is strikingly slow and only moderately enhanced by either homo- or heteroexchange. A part of taurine release evoked by potassium depolarization from brain slices and synaptosomes is clearly calcium dependent when the enhancement of release--to a great extent from glial cells--induced by calcium-free media and calcium chelators is properly taken into account in evaluation. Sodium-free medium is the most effective means in provoking taurine efflux. It is suggested that normally the transmembrane sodium gradients aid in maintaining the high intracellular taurine concentrations.

Animals↗
PubMed1985

Properties of sodium-independent taurine binding to brain synaptic membranes.

The sodium-independent taurine binding to twice Triton treated brain membranes characterized here was reversible, temperature-insensitive and saturable with a broad pH optimum, being thus characteristic of a synaptic receptor site. Only one type of binding site with a rather low maximal capacity was detected. Furthermore, binding exhibited properties of positive cooperativity, indicating that two or more taurine molecules possibly interact at a binding site. Both GABA and glycine as well as their agonists and antagonists strongly displaced taurine binding. The novel anticonvulsive taurine derivatives wee also effective displacers. The relevance of the binding observed in vitro to the possible synaptic receptors for taurine in vivo still remains to be determined.

Animals↗