Chronic administration of lithium modulates tryptophan transport by changing the properties of the synaptosomal plasma membrane.

The effect of chronic administration of lithium salts on the sodium dependent high-affinity system for tryptophan uptake was examined in plasma membrane vesicles derived from rat brain. Tryptophan transport was measured as a function of the temperature, Arrhenius plots of the data were prepared, and the apparent energies of activation were computed. Both plots were biphasic, the transition temperature decreasing from 23 degrees C in control animals to 18 degrees C in treated rats.

Effects of systematically administered lithium on tryptophan transport and exchange in plasma-membrane vesicles isolated from rat brain.

The effect of lithium on the sodium-dependent high-affinity system for tryptophan uptake was examined in plasma membrane vesicles derived from rat brain. We demonstrated that Na+ could be replaced by lithium in the external medium and the presence of lithium produced an increase in the Vmax of the tryptophan transport whereas it had no significant effect on the Km for the substrate. Plasma membrane vesicles derived from synaptosomes obtained from long-term lithium-treated rats are able to accumulate tryptophan to a greater extent than normal rats and maintain a more negative membrane potential than controls.

Stoichiometry of sodium- and chloride-coupled glycine transport in synaptic plasma membrane vesicles derived from rat brain.

The stoichiometric properties of the glycine transporter were studied in synaptic plasma membrane vesicles from rat brain. The present results, together with previous data from our laboratory, allow us to suggest a stoichiometry of 2 Na+ and 1 Cl- per glycine zwitterion for the translocation cycle catalyzed by the glycine carrier. We propose a kinetic model with an ordered mechanism for the binding/debinding of solutes.

Characterization of glycine uptake in plasma membrane vesicles isolated from cultured glioblastoma cells.

C6 glioblastoma cells in culture were employed to isolate plasma membrane vesicles. After disruption of the glioblastoma cells by homogenization, membrane fractions were obtained by centrifugation on a discontinuous Ficoll density gradient. Fragmented membranes were found mainly in vesicular form.

Beta-alanine transport in synaptic plasma membrane vesicles from rat brain. Efflux, exchange and stoichiometry.

The efflux and exchange of beta-alanine were studied in synaptic plasma membrane vesicles from rat brain. The mechanism of beta-alanine translocation has been probed by comparing the ion dependence of net efflux to that of exchange. Dilution-induced efflux requires the simultaneous presence of internal sodium and chloride ions while influx is dependent on the presence of these two ions on the outside [Zafra, F.

Tyrosine transport into isolated rat brain synaptosomes. Ionic dependence and kinetic studies.

The ionic dependence and kinetics of the uptake of L-tyrosine into isolated rat brain synaptosomes has been investigated. L-Tyrosine has been found to enter the synaptosomes through three different transport systems showing distinct ionic requirements and kinetic characteristics. The one with the lowest affinity for tyrosine (Km 0.

Efflux and exchange of glycine by synaptic plasma membrane vesicles derived from rat brain.

The influx and exchange of glycine were studied in synaptic plasma membrane vesicles isolated from rat brain. The vesicles were loaded with [U-14C]glycine by active transport driven by an Na+ as well as a Cl- gradient (out greater than in). Dilution-induced efflux requires the simultaneous presence of internal Na+ and Cl-.

Developmental studies on the uptake of tyrosine by synaptosomes and plasma membrane vesicles derived from rat brain. Effect of thyroid hormones.

The uptake of L-tyrosine at various stages of development was examined in synaptosomes and in plasma membrane vesicles derived from rat brain. The total uptake has two components, Na+-dependent and Na+-independent, respectively. The Na+-dependent component of the transport system appears around the 5th postnatal day and increases with age.

Ontogenetic studies on tryptophan transport into plasma membrane vesicles derived from rat brain synaptosomes: effect of thyroid hormones.

The uptake of tryptophan at various stages of development was examined in plasma membrane vesicles derived from rat brain. The total uptake has two components Na+-dependent and Na+-independent respectively. The Na+-dependent component of the transport system appears around the 5th postnatal day and increases with the age.

Thromboembolism with low profile bioprosthesis.

Low profile bioprosthesis late follow-up indicates a low incidence of thromboembolism. For the entire series of 415 consecutively operated patients (rigid and flexible stents) the actuarial probability of freedom at 6 years is 90.3% (87.

beta-Alanine transport into plasma membrane vesicles derived from rat brain synaptosomes.

Transport of beta-alanine has been demonstrated in membrane vesicles isolated from rat brain, using artificially imposed ion gradients as the sole energy source. The uptake of beta-alanine is strictly dependent on the presence of Na+ and Cl- in the medium, and the process can be driven either by an Na+ gradient (out greater than in) or by a Cl- gradient (out greater than in) when the other essential ion is present. The process is stimulated by a membrane potential (negative inside) as demonstrated by the effect of ionophore valinomycin and anions with different permeabilities.

Tryptophan transport into plasma membrane vesicles derived from rat brain synaptosomes.

Tryptophan uptake by membrane vesicles derived from rat brain was investigated. The uptake is dependent on the Na+ gradient [Na+] outside greater than [Na+] inside, and is maximal when both Na+ and Cl- are present. The uptake represents transport into an osmotically active space and not a binding artifact, as indicated by the effect of increasing the medium osmolarity.

Inhibition by L-phenylalanine of tryptophan transport by synaptosomal plasma membrane vesicles: implications in the pathogenesis of phenylketonuria.

Phenylalanine is accumulated in the genetically linked deficiency phenylketonuria. The effect of L-phenylalanine on the transport of tryptophan was studied using membrane vesicles from rat-brain synaptosomes. Phenylalanine at similar concentrations to those found in phenylketonuric patients competitively inhibits tryptophan uptake, with a Ki of the same order as the Km for tryptophan.

Inhibition by L-phenylalanine of tyrosine transport by synaptosomal plasma membrane vesicles: implications in the pathogenesis of phenylketonuria.

The effect of L-phenylalanine on the transport of tyrosine was studied using membrane vesicles from rat brain synaptosomes. Phenylalanine, which is accumulated in phenylketonuria, competitively inhibits tyrosine uptake at concentrations similar to those found in phenylketonuric patients, with a Ki of the same order of the Km for tyrosine. This inhibition could be responsible for the depletion of catecholamines observed in phenylketonuria.

The low profile bioprosthesis: results with 491 valves implanted in 453 patients for up to 5 years.

This report summarizes results of the first 453 consecutive patients who had 491 low profile bioprostheses implanted at the Italian Hospital in Buenos Aires over a 5-year period. During this time, with the goal of long-term durability, the valve mounting technique was slightly modified, whereas the materials and design of the annulus underwent more extensive changes.

[Pathogenesis of cerebral dysfunction in phenylketonuria].

Although the enzymatic etiology and the link between this and the accumulation of phenylalanine and its metabolites in phenylketonuria has been amply established, the pathogenesis of the brain dysfunction accompanying this inherited metabolic disease is still under research. Effects of phenylalanine and its metabolites, some leading to irreversible defective structural features in the nervous system, and others to reversible defective neurotransmission, are described as responsible of the mental retardation and other neurological and behavioural symptoms characteristic of phenylketonuria.

[Inhibition of L-tyrosine transport in isolated synaptosomes from rat brain in the presence of L-tryptophan and L-phenylalanine].

The high-affinity transport system of L-tyrosine into rat brain synaptosomes is competitively inhibited by L-Tryptophan and by L-Phenylalanine. These results support the common carrier hypothesis for the transport of aromatic amino acids into the neuron and suggest that the high levels of phenylalanine present in phenylketonuria could be responsible for the impairment synthesis of neurotransmitter monoamines found in brain of patients affected by that disease.

L-Aspartate transport into plasma membrane vesicles derived from rat brain synaptosomes.

Aspartate uptake by membrane vesicles derived from rat brain was investigated. The uptake is dependent on a Na+ gradient ([Na+] outside greater than [Na+] inside). Active transport of aspartate is strictly dependent upon the presence of sodium and maximal extent of transport is reached when both Na+ and Cl- ions are present.

Glycine transport into plasma-membrane vesicles derived from rat brain synaptosomes.

1. Transport of glycine has been demonstrated in membrane vesicles isolated from rat brain, using artificially imposed ion gradients as the sole energy source. 2.

Tyrosine transport by membrane vesicles isolated from rat brain.

Tyrosine uptake by membrane vesicles derived from rat brain has been investigated. The uptake is dependent on an Na+ gradient ([Na+]outside greater than [Na+]inside). The uptake is transport into an osmotically active space and not a binding artifact as indicated by the effect of increasing the medium osmolarity.

Effect of thyroid hormones on the malic enzyme activity in rat brain during development.

Changes in the development pattern of cytoplasmic and mitochondrial malate dehydrogenase (decarboxylating; NADP+) activity in the brain of hypothyroid rats and the effect of triiodothyronine on the enzyme activity have been investigated. Hypothyroid rats showed lower malate dehydrogenase activity than controls during the suckling period. Results suggest that thyroid hormones promote the development of malic enzyme in the brain.

Effect of thyroid hormones on the 3-oxo acid CoA-transferase activity in rat brain during development.

The changes in the developmental pattern of 3-oxo acid CoA-transferase activity in the brain of hypothyroid rats and the effect of triiodothyronine on this enzyme activity have been investigated. Hypothyroid rats showed lower activity than controls during the suckling period. However, higher enzyme levels were found in treated rats after weaning in contrast to control animals.