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Biomedical subjects

S S Oja

Publications and source records attributed to S S Oja.

At least 163 records · Page 9Linked to original sources

The accumulation of 2-aminoisobutyric acid in the costal and lumbar parts of the phrenectomized rat diaphragm in vitro.

The accumulation of 2-aminoisobutyric acid initially increased in denervated costal and lumbar parts of the rat hemidiaphragm after both unilateral and bilateral phrenectomy, followed by a later gradual decrease. The enhancement of accumulation was invariably higher in the costal than in the lumbar part. The accumulation was initially lower in bilaterally than in unilaterally phrenectomized hemidiaphragms, but the relationship was reversed after 72 h due to a faster reattenuation of the enhancements in unilaterally phrenectomized diaphragms.

Aminoisobutyric Acids↗

Transport of leucine, lysine, glycine and aspartate in neuroblastoma C1300 and glioma C6 cells.

Non-saturable penetration and the V and Km constants of saturable influx of leucine, lysine and glycine were always greater in cultured neuroblastoma (C1300) than in glioma (C6) cells. Aspartate uptake was detected only in glioma cells. Unstimulated efflux of the amino acids was initially fast in both cell types but soon slowed down. The efflux of glycine and aspartate exhibited no heteroexchange, the efflux of lysine was stimulated by extracellular leucine and that of leucine slightly by lysine and glycine but only in glioma cells.

Animals↗

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↗

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↗

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↗

Cerebral cortex slices in sodium-free medium: depletion of synaptic vesicles.

Rat cerebral cortex slices superfused for 5 min in sodium-free medium after 30-min stabilization and 25-min superfusion periods in sodium-containing medium displayed a well-preserved tissue structure and mostly intact neurons and glial cells. Electron-microscopic morphometry showed the number of presynaptic terminals containing few (less than or equal to 10) vesicles to increase 3-fold after the 5-min depletion of sodium. The 90-min sodium depletion resulted in increased swelling and an additional decrease in synaptic vesicles. The results show that from a morphological point of view the substitution of sodium by choline with brain slice techniques is an eminently suitable method for studies on synaptic neurochemistry.

Animals↗

Stimulation of amino acid accumulation in neuroblastoma and astrocytoma cells by L-histidine.

Uptake of amino acids by cultured neuroblastoma and astrocytoma cells was studied in the presence and absence of L-histidine. Intracellularly accumulated histidine was assumed to induce accumulation of radioactively labeled amino acids from medium by means of exchange transport. Neuroblastoma cells accumulated more histidine than astrocytoma cells and were more sensitive to the enhancement of uptake of other large neutral amino acids by histidine. Histidine also increased glutamic acid uptake in astrocytoma cells, but reduced it in neuroblastoma cells. The greatest differences between the cell lines in amino acid uptake without histidine were found with acidic amino acids (astrocytoma cells accumulated them more than neuroblastoma cells) and with taurine (the reverse was found). The uptake and exchange mechanisms for some neutral and acidic amino acids may thus be dissimilar in the plasma membranes of cultured cells of neuronal and glial origin.

Amino Acids↗

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↗

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↗

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↗

Synthesis and anticonvulsant properties of some 2-aminoethanesulfonic acid (taurine) derivatives.

A series of 2-acylaminoethanesulfonamides were synthesized by treating the corresponding sulfonyl chlorides with ammonia, a primary, or a secondary amine. A few compounds displayed marked anticonvulsant activity in mice when tested for their potency in the maximal electroshock seizure test. The piperidino, benzamido, phthalimido, and phenylsuccinylimido derivatives were active, whereas the succinylimido, saccharinylimido, and norbornenedicarboxylimido compounds showed no activity. The interference with the sodium-independent taurine binding to mouse brain synaptic membranes was assessed to elucidate the possible mode of anticonvulsant action.

Animals↗

Calcium chelators enhance the efflux of taurine from brain slices.

Efflux of exogenous [3H]taurine from superfused slices of cerebral cortex of rat was enhanced by the calcium chelators EDTA and EGTA and by large concentrations of unlabelled taurine and histidine. The enhancement by EDTA and EGTA could be totally blocked by excess calcium, but that by the amino acids only partially. The enhancement of spontaneous taurine release in the absence of calcium complicates the assessment of the calcium dependence of evoked taurine release.

Animals↗

Modulation of noradrenaline uptake and release by taurine in rat cerebral slices.

The effects of taurine on the uptake and release of noradrenaline were studied in forebrain slices from control rats and from rats treated with a taurine-free diet supplemented with 2-guanidinoethanesulphonate. Exogenous taurine slightly increased noradrenaline uptake in slices from untreated rats. There were no significant effects by exogenous taurine on spontaneous efflux of noradrenaline. The potassium-stimulated noradrenaline release was enhanced by taurine from frontal cortical slices and suppressed from occipital slices but only in the diet group, in which the endogenous brain taurine concentration had been lowered to one-half of the control concentration. It is suggested that taurine may act via presynaptic alpha-adrenoceptors and/or modify the availability of calcium for the stimulus-secretion coupling process.

Animals↗

Comparison of two superfusion systems for study of neurotransmitter release from rat cerebral cortex slices.

Depolarization-induced release of [3H]gamma-aminobutyric acid (GABA) and [3H]noradrenaline (NA) from rat cerebral cortex slices was studied in two superfusion systems: one with stationary and the other one with continuously shaken slice compartments. Calcium-dependent depolarization-induced release of GABA and NA could be demonstrated only with shaken slices. GABA, but not NA, could also be released by high K+ media and veratridine from stationary slices. Synaptic transmitter releasing mechanisms are apparently damaged in stationary slices, possibly due to impaired energy metabolism.

Adenosine Diphosphate↗

Effect of L-tryptophan supplementation on ischemic pain.

The synthesis of neurotransmitter amines in mammalian brain is known to respond to changes in precursor availability. After dietary manipulation including L-tryptophan supplementation 3 subjects out of 11 showed a significant reduction of experimentally induced ischemic pain. It is suggested that dietary manipulation aimed at an increase in central nervous system serotonin can alter pain perception in some individuals.

Adult↗