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Biomedical subjects

M Banay-Schwartz

Publications and source records attributed to M Banay-Schwartz.

At least 55 records · Page 3Linked to original sources
PubMed1983

Glycine: a possible role in lithium's action and affective illness.

In addition to its incorporation into proteins, glycine functions as both a regulator of one-carbon metabolism and as an inhibitory neurotransmitter. Clinical recognition of the hyperglycinemias and reported elevations of erythrocyte glycine concentrations in patients with bipolar disorders have implicated this amino acid in the etiopathology of some neuropsychiatric disorders. Moreover, chronic lithium administration, an almost specific intervention for the treatment and prophylaxis of bipolar disorders, has been shown to induce elevations in brain and erythrocyte glycine levels. In view of glycine's complex metabolic interrelationships and neurotransmitter function, additional research exploring its possible role in either affective illness or lithium's action is indicated.

Amino Acid Metabolism, Inborn Errors↗
PubMed1982

Erythrocyte glycine in depressed, hypomanic, and euthymic bipolar patients treated with lithium carbonate.

Red blood cell (RBC) glycine levels were examined in 27 bipolar patients, treated with lithium carbonate for a minimum of 8 months, who were either hypomanic, depressed, or euthymic in their mood. We found no difference in the RBC glycine or in the RBC: plasma glycine ratio between the hypomanic, depressed, or euthymic patients (P less than 0.1). There were statistically significant differences in RBC glycine levels in lithium-treated euthymic patients and normal controls. There was a strong positive correlation between serum lithium levels and both RBC glycine levels and the RBC: plasma glycine ratio.

Adult↗
PubMed1982

Lithium: effect on [3H]spiperone binding, ionic content, and amino acid levels in the brain of rats.

After prolonged treatment of rats with lithium (pellets, 0.21% lithium carbonate, or 0.5 mg/ml lithium chloride in drinking water) for three months, the level of lithium in plasma was 0.87 meq/liter; in several brain regions, between 1.06-1.39 mueq/g wet weight. The content of sodium and potassium inthe plasma was normal. The level of potassium in the brain regions tested increased by 13-30% and that of sodium by about 10%. Glycine levels increased significantly in all the regions (cerebral cortex, midbrain, cerebellum, and spinal cord). In the cerebellum GABA was also increased, while glutamine was decreased. In midbrain, apart from increases in glycine levels, alanine, valine, GABA and lysine were also increased. In the spinal cord, glutamic acid was also increased. Changes were largely in the putative neurotransmitters. Long-term treatment with lithium also influenced the high-affinity binding of [3H] spiperone in the cerebral cortex and corpus striatum. Two specific binding sites were found in both brain regions; the main change was the reduction in the lower affinity binding site (B max 2).

Amino Acids↗
PubMed1982

Effects of prenatal administration of nicotine on amino acid pools, protein metabolism, and nicotine binding in the brain.

The effects of nicotine on brain protein metabolism and on the properties of the nicotine binding site were investigated in newborn animals exposed to nicotine during gestation. Brain protein synthesis rates measured in vivo were lower by 18% in newborn of treated animals. Protein degradation rates measured in vitro in the presence of nicotine were lower by 13%. The effect was specific for L-(-)nicotine, since D-(+)nicotine, nicotinic acid, or nicotinamide had no effect on degradation rates. Newborn brain amino acid levels, mainly nonessential amino acids and amino acids of putative neurotransmitter function, were changed somewhat; an increase in the level of taurine (13%), threonine (21%), serine (35%) and glycine (35%), and a decrease in lysine (14%) was observed in the offspring of nicotine treated animals (0.5 mg/kg, s.c., 2 x daily throughout gestation). These changes could not account for the decrease in protein metabolism. Nicotine binding was higher by 25% in the offspring of animals exposed to nicotine during gestation. No such increase was found after treatment of adult rats with nicotine, indicating that the properties of the nicotine binding site change with age.

Aging↗
PubMed1982

Naloxone, tardive dyskinesia, and endogenous beta-endorphin.

The subjects were 13 psychiatric inpatients with tardive dyskinesia. Each subject participated in two sessions. Either naloxone (10 mg) or placebo was administered intravenously during each session. In a subset of subjects (n = 7), blood samples for beta-endorphin were drawn before and at 30 and 60 minutes after the injection. The Abnormal Involuntary Movement Scale was administered before and at 10, 20, 40, 60, 120, and 360 minutes after the injection. Double-blind procedures were maintained throughout the experiment. Neither naloxone nor placebo had any appreciable effect on the involuntary movements. Naloxone elicited a significant increase in the plasma beta-endorphin.

Adult↗
PubMed1981

Effect of lithium and sodium ions on opiate- and dopamine-receptor binding.

The effects of lithium and sodium were studied in the corpus striatum and cerebral cortex of rats. Lithium was inhibitory at low concentrations but at 20 mM it increased the binding of [G-3H]naloxone (specific activity 15.6 Ci/mmol). Sodium stimulated the high-affinity binding of this compound. Membranes obtained from the rats treated with lithium showed lower specific binding of both [3H]naloxone and [3H]DHM. Binding of [3H]d-alanine Leu-enkephalin was not changed in the brains of lithium-treated rats, but that of [3H]-spiroperidol was lowered. Cerebral cortex and striatum of lithium-treated rats had a decreased apparent dissociation constant and a lower receptor concentration of naloxone binding sites.

Animals↗
PubMed1980

Enkephalin degradation stimulated by captopril.

Changes in the rates of degradation of Met- and Leu-enkephalin by brain aminopeptidase were measured by UV absorption after high-pressure liquid chromatography. The cleavage of enkephalin paralleled the generation of tyrosine. Captopril (SQ 14,225) stimulated enzyme activity, to a greater extent with Met- than with Leu-enkephalin. Pro-His-Pro-NH2, histidine, and histamine stimulated enkephalin aminopeptidase approximately twice as much as captopril. The sulfhydryl group of captopril was not the only factor in its effect. The addition of captopril did not change the pH optimum, and it stimulated enkephalin degradation between 25 and 50 degrees C.

Aminopeptidases↗
PubMed1980

Nucleoside uptake by slices of mouse brain.

The properties of the uptake of nucleosides and nucleotides by brain cells were examined in slices of mouse brain. Of the compounds tested, adenine and adenosine had the most rapid uptake and reached the highest levels. Uptake was mediated, as shown by saturability and strong inhibition, by low temperature, or by cyanide, and was only partially sodium- or calcium-dependent. The inhibition pattern by analogues indicated the presence of several uptake systems (possibly four), as shown by differences between adenine and guanine uptake, between adenine and adenosine uptake, and between adenosine and cytidine uptake. The properties of uptake systems for nucleotides and nucleosides were somewhat different from those for amino acids.

Animals↗
PubMed1978

Decrease in cerebral protein synthesis on a low protein diet.

When rats are put on a diet that is low in protein or contains no protein, decrease in brain weight can be observed. Changes in adults are minimal. In the young there is a 10--30% decrease in cell number and protein content; the cell size (protein per cell) does not change significantly. The change is greater, the earlier the diet is started and the more severe the protein dificiency is. The longer the malnutrition period lasts, the smaller is the recovery to normal values on subsequent control diets. Amino acid incorporation in the brain decreased 10--30% under these experimental conditions; it seems the decrease was to a great extent in the more slowly metabolized protein pool. Changes in other organs were greater; for example, in liver the decrease was up to 75% under similar conditions. The changes in the brain were heterogeneous; there were regional differences, and not all proteins were affected to the same degree; choline acetyltransferase was not affected. Cellular amino acid transport as studied with incubated slices of brain was not altered under these conditions.

Animals↗
PubMed1976

Energetics of low affinity amino acid transport into brain slices.

It appears possible to dissect and study some of the potential energy sources for amino acid transport in brain slices despite the apparent complexity of the tissue in comparison to that of isolated bacterial vesicles23. The uptake capability of the tissue may be inadvertently damaged in some experimental protocols so that very special controls must be used to ensure that the treatment did not somehow inactivate the very mechanism that thereafter will be tested. We have presented some evidence that brain slice amino acid transport may not be obligatorily linked to glycolysis, ATP levels, Na+, K+-ATPase activity, K+ levels or direction of flux, or to Na+ flux. However, the energy source linkage for different amino acids appears to be rather specific, so that further generalizations are difficult to sustain. For instance, the incubation media and conditions we describe here were experimentally adjusted to maximize uptake of D-glu or alpha-AIB in the absence of glucose, or in lowered K+ or Na+. Therefore, these procedures, the results of which directly challenge some common assumptions regarding the energy basis for active transport in brain slices, probably will not be universally extensible to all other actively transported amino acids.

Adenosine Triphosphate↗