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Liane N Rotta

Publications and source records attributed to Liane N Rotta.

15 recordsLinked to original sources
PubMed2006

Effect of 2-deoxy-D-glucose on aminoacids metabolism in rats' cerebral cortex slices.

We studied the effect of different concentrations of 2-deoxy-D-glucose on the L-[U-14C]leucine, L-[1-14C]leucine and [1-14C]glycine metabolism in slices of cerebral cortex of 10-day-old rats. 2-deoxy-D-glucose since 0.5 mM concentration has inhibited significantly the protein synthesis from L-[U-14C]leucine and from [1-14C]glycine in relation to the medium containing only Krebs Ringer bicarbonate. Potassium 8.0 mM in incubation medium did not stimulate the protein synthesis compared to the medium containing 2.7 mM, and at 50 mM diminishes more than 2.5 times the protein synthesis compared to the other concentration. Only at the concentration of 5.0 mM, 2-deoxy-D-glucose inhibited the CO2 production and lipid synthesis from L-[U-14C] leucine. This compound did not inhibit either CO2 production, or lipid synthesis from [1-14C]glycine. Lactate at 10 mM and glucose 5.0 mM did not revert the inhibitory effect of 2-deoxy-D-glucose on the protein synthesis from L-[U-14C]leucine. 2-deoxy-D-glucose at 2.0 mM did not show any effect either on CO2 production, or on lipid synthesis from L-[U-14C]lactate 10 mM and glucose 5.0 mM.

Animals↗
PubMed2004

Increased locomotor response to amphetamine, but not other psychostimulants, in adult mice submitted to a low-protein diet.

Protein malnutrition results in a variety of brain dysfunctions, ultimately affecting cognitive functions. The effects of protein malnutrition in brain response to psychostimulants have been less studied in adult animals. We therefore aimed to study the response to psychoactive drugs on the locomotor activity (a behavior paradigm) of adult protein malnourished mice. Two-month-old mice were divided in two groups: (a) low-protein group (LP), which received 6% of protein diet, and (b) a control group that received a 25% of protein diet. After 3 months, they were tested for locomotor activity after an i.p. injection of one of psychoactive drugs: D-amphetamine (5.0 mg/kg), apomorphine (2.0 mg/kg), dizocilpine (0.25 mg/kg), or caffeine (30 mg/kg). Mice submitted to the LP diet presented prolonged induction of hyperlocomotion caused by amphetamine (about 350% between 90 and 180 min post drug injection as compared with well-nourished mice, p<0.01) but presented unaltered response to apomorphine, caffeine, and dizocilpine. These data point to altered catecholamine metabolism induced by protein restriction in adult mice. The results are discussed based on previous works, presenting theoretical hypotheses about the possible mechanisms involved in the present findings.

Amphetamine↗
PubMed2004

Effects of undernutrition on glycine metabolism in the cerebellum of rats.

Undernutrition is a worldwide problem affecting millions of unborn and young children during the most vulnerable stages of brain development. Total restriction of protein during the perinatal period of life can alter the development of the mammalian fetus and have marked repercussions on development of the central nervous system (CNS). The brain is vulnerable to undernutrition with altered morphologic and biochemical maturation, leading to impaired functions. The focus of this study is to investigate [U-14C]glycine metabolism in undernourished rats submitted to pre- and postnatal protein deprivation (diet: 8% protein with and without addition of L-methionine; control group: 25% protein). Although undernutrition produced a reduction in cerebellar weight and alterations in the DNA concentration, the present study shows that glycine metabolism in this structure is partially protected because the undernourished group with L-methionine did not show modifications in glycine metabolism at all ages studied. However, L-methionine deficiency alters glycine metabolism at 7 and 21 days, but in the adult age both undernourished groups presented no differences in oxidation to CO2, conversion to lipids and incorporation into protein from glycine, compared to the control group.

Aging↗
PubMed2004

In vitro effects of D-2-hydroxyglutaric acid on glutamate binding, uptake and release in cerebral cortex of rats.

Neurological dysfunction is common in patients with D-2-hydroxyglutaric aciduria (DHGA). However, the mechanisms underlying the neuropathology of this disorder are far from understood. In the present study, we investigated the in vitro effects of D-2-hydroxyglutaric acid (DGA) at various concentrations (0.1-1.0 mM) on various parameters of the glutamatergic system, namely the basal and potassium-induced release of L-[3H]glutamate by synaptosomal preparations, Na(+)-dependent L-[3H]glutamate uptake by synaptosomal preparations and Na(+)-independent L-[3H]glutamate uptake by synaptic vesicles, as well as of Na(+)-independent and dependent L-[3H]glutamate binding to synaptic plasma membranes from cerebral cortex of male adult Wistar rats. We observed that DGA significantly increased synaptosomal L-[3H]glutamate uptake, without altering the other parameters. Although these findings do not support a direct excitotoxic action for DGA since the metabolite did not affect important parameters of the main neurotransmission system, they do not exclude a direct action of DGA on NMDA or other glutamate receptors. More comprehensive studies are therefore necessary to evaluate the exact role of DGA on neurotransmission.

Animals↗
PubMed2004

Characterization of imido [8-(3)H] guanosine 5'-triphosphate binding sites to rat brain membranes.

Besides their well-defined intracellular roles in transmembrane signals transduction, guanine derivatives play important roles by acting from the outside of neural cell membranes. These roles are mediated by two different pool sites in cell membranes: G proteins, which bind to specific (GDP and GTP) intracellular guanine derivatives, and sites that bind to extracellular guanine derivatives. In this study we investigated some methodological characteristics of both guanine derivatives binding sites (intracellular and extracellular) in rat brain neural membranes. By investigating the binding of a poorly hydrolyzed GTP analogue and the adenylate cyclase activity in neural membranes, we observed some distinctiveness of guanine derivatives binding sites: stability to washing procedures (extracellular) and modulation of adenylate cyclase activity (intracellular). These results allow dealing with each site separately, which could be useful for discriminating the roles of extracellular and intracellular guanine derivatives in the central nervous system.

Adenylyl Cyclases↗
PubMed2004

High extracellular K+ levels stimulate acetate oxidation in brain slices from well and malnourished rats.

We investigated the effect of high (12, 20, and 50 mM) extracellular K+ concentrations ([K+]0) on [U-14C] acetate oxidation to CO2 in cerebral cortex slices of control and perinatal malnourished rats. High [K+]o increased the acetate oxidation, compared with a medium containing 2.7 mM [K+]0. By investigating the mechanisms involved in this stimulation, it was shown that (i) ouabain (1 mM) and monensin (10 microM) prevented this increase; (ii) in a medium with physiological [K+]0 (2.7 mM), the decreasing of [Na+]0 stimulated acetate oxidation. These results suggest that the stimulatory effect of [K+]0 on acetate oxidation was due to the decreasing of Na1 levels. Considering that malnutrition could alter the activity of Na+,K(+)-ATPase and/or other pertinent proteins, its effect on acetate oxidation was investigated. The malnutrition, which altered the body and cerebral weight of rats, did not modify the acetate oxidation in any protocol.

Acetates↗
PubMed2003

Serum and liver lipids in rats and chicks fed with diets containing different oils.

OBJECTIVES: Because dietary fat composition is determinant for serum cholesterol level, which is related to cardiovascular disease, we evaluated the effects of diets containing saturated (coconut oil) or polyunsaturated fatty acids (soybean oil) supplemented or not with dietary cholesterol on serum and liver lipid composition in two animal species. METHODS: Male Wistar rats (21 d old) were assigned to one of seven groups and fed with commercial diet or diets containing 5% or 20% soybean oil or 20% coconut oil with or without 1% cholesterol. Chicks were assigned to one of four groups and fed with diets containing 15% soybean oil or 15% coconut oil with or without 1% cholesterol. RESULTS: In rats, the accumulations of hepatic cholesterol and triacylglycerols were higher in the group fed 20% soybean oil and 1% cholesterol than in the group fed 20% coconut fat and 1% cholesterol. The highest serum levels of cholesterol and triacylglycerols were observed in the group fed coconut oil and cholesterol, compared with the group fed soybean oil and cholesterol. Triacylglycerol, high-density lipoprotein, and total cholesterol serum levels increased with diet containing coconut oil and cholesterol. In chicks, the highest hepatic cholesterol accumulation occurred in the group fed 15% coconut fat and 1% cholesterol. Total and high-density lipoprotein cholesterol levels increased with diet containing coconut oil and cholesterol, although none of these diets modified serum triacylglycerol levels. CONCLUSIONS: The type of experimental animal model and the diet composition influence lipid metabolism.

Animals↗
PubMed2003

Effects of undernutrition on glutamatergic parameters in rat brain.

Early restriction of nutrients during the perinatal period has marked repercussions on CNS ontogeny, leading to impaired functions. This study investigated the effects of pre- and postnatal (up to 75 days) undernutrition (diet: 8% protein; normonourished group: 25% protein) on some glutamatergic and behavioral parameters of rats. Undernutrition reduced: (i) seizures caused by ICV quinolinic acid (QA) administration; (ii) Na-independent [3H]glutamate binding in cell plasma membranes of cerebral cortex, and (ii) basal [3H]glutamate release from synaptosomal preparation. Behavioral parameters related to locomotion, anxiety, or memory were not affected. These results indicate that our model of undernutrition decreased the sensitivity to QA as convulsing agent and point to some putative glutamatergic parameters involved in this effect.

Animals↗
PubMed2003

Effects of L-2-hydroxyglutaric acid on various parameters of the glutamatergic system in cerebral cortex of rats.

L-2-Hydroxyglutaric acid (LGA) accumulates and is the biochemical hallmark of the neurometabolic disorder L-2-hydroxyglutaric aciduria (LHGA). Although this disease is predominantly characterized by severe neurological findings and pronounced cerebral atrophy, the pathomechanisms of brain injury are virtually unknown. In the present study, we investigated the effect of LGA (0.1-1 mM) on various parameters of the glutamatergic system, namely the basal and potassium-induced release of L-[3H]glutamate by synaptosomal preparations, Na(+)-dependent L-[3H]glutamate uptake by synaptosomal preparations and Na(+)-independent L-[3H]glutamate uptake by synaptic vesicles, as well as of L-[3H]glutamate binding to synaptic plasma membranes from cerebral cortex of male adult Wistar rats. We observed that LGA significantly increased L-[3H]glutamate uptake into synaptosomes and synaptic vesicles, without altering synaptosomal glutamate release and glutamate binding to synaptic plasma membranes. Although more comprehensive studies are necessary to evaluate the exact role of LGA on neurotransmission, our findings do not support a direct excitotoxic action for LGA. Therefore, other abnormalities should be searched for to explain neurodegeneration of LHGA.

Animals↗
PubMed2002

Utilization of energy nutrients by cerebellar slices.

We performed an ontogenetic study about the utilization of glycine, glutamine, beta-hydroxybutyrate and glycerol as energy nutrients by rat cerebellum slices. Production of CO2 from glycerol and glutamine increased with the animals' age and glutamine was the most used nutrient for CO2 production. In adult age, glutamine oxidation to CO2 was 15 to 35 times higher than all other nutrients studied. CO2 production from glycine decreased markedly with age and 10 day-old rats showed an oxidation 7.5 times higher than that of adult rats. At fetal age and at 10 postnatal days, glycine oxidation to CO2 was only 2 times lower than glutamine oxidation to CO2. Lipid synthesis from beta-hydroxybutyrate was highest in adult rats. We did not observe any difference in the utilization of beta-hydroxybutyrate between slices of cerebral cortex and cerebellum at the ages of 10 days and adult. The main nutrients used for lipid synthesis were glycerol and beta-hydroxybutyrate.

3-Hydroxybutyric Acid↗
PubMed2002

Exposure to ebselen changes glutamate uptake and release by rat brain synaptosomes.

We investigated effects of Ebselen, diphenyl diselenide (PhSe)2 and diphenyl ditelluride (PhTe)2 on [3H]glutamate uptake and release by brain synaptosomes. Ebselen after acute exposure inhibited K+-stimulated [3H]glutamate release by brain synaptosomes. (PhSe)2 and (PhTe)2 did not change [3H]glutamate release by brain synaptosomes. Ebselen, (PhSe)2 and (PhTe)2 had no significantly effects on [3H]glutamate uptake after acute exposure. In vitro, Ebselen (100 microM) inhibited [3H]glutamate release and uptake. (PhSe)2 had no significant effect, while (PhTe)2 (100 microM) inhibited [3H]glutamate uptake by brain synaptosomes. In vitro, (PhSe)2, (PhTe)2 and Ebselen caused a significant inhibition of [3H]glutamate uptake by brain synaptic vesicles in vitro. The results demonstrated that organochalcogenides have a rather complex effect on glutamate homeostasis depending on the compound and the schedule of exposition. We propose that the neuroprotective action of Ebselen can be related, in addition to its glutathione peroxidase-like and antilipoperoxidative activity, to a direct interaction with the glutamatergic system by reducing K+-evoked glutamate release.

Animals↗
PubMed2002

Ontogenetic study of the effects of energetic nutrients on amino acid metabolism of rat cerebral cortex.

We studied the effect of various energetic nutrients on metabolism of L-[U-14C]leucine and [1-14C]glycine in cerebral cortex of rats at different ages. At gestational age, glucose and lactate stimulated protein synthesis from L-[U-14C]leucine and [1-14C]glycine and from L-[U-14C]leucine, respectively; glucose, beta-OH-butyrate and lactate stimulated lipid synthesis from L-[U-14C]leucine. At 10 days of age, glucose, mannose, and fructose stimulated protein synthesis, and glucose and mannose stimulated oxidation to CO2 as well as lipid synthesis from L-[U-14C]leucine. In adult rats, glucose, mannose, and fructose stimulated protein synthesis from L-[U-14C]leucine and [1-14C]glycine; glutamine also markedly decreased the oxidation of L-[U-14C]leucine and [1-14C]glycine in 10-day-old and adult rats.

Aging↗
PubMed2002

Effect of undernutrition on GMP-PNP binding and adenylate cyclase activity from rat brain.

1. Undernutrition is an insult that affects brain development and functioning. Considering that signaling through metabotropic receptors/G proteins is critical for normal synaptic transmission and contributes to CNS development and synaptic plasticity, the present study investigated the effects of pre- and postnatal protein deprivation (diet: 8% protein; normonourished group: 25% protein) on brain signal transduction by G proteins. 2. Undernutrition decreased the [3H] GMP-PNP binding to G proteins and AC activity, in neural plasma synaptic membranes of 21- and 75-day-old rats. This effect was less pronounced or even absent in old rats. 3. Ontogenetically, the dietary treatment effect might be interpreted as a retarded development associated with protein malnutrition.

Adenylyl Cyclases↗
PubMed2002

A ketogenic diet increases protein phosphorylation in brain slices of rats.

Ketogenic diets have been used to treat seizure disorders of children and recently it was shown to increase the drug-induced seizure threshold in rats. Protein phosphorylation is a major regulatory mechanism of signal transduction that has been implicated in modulating neuronal excitability. We investigated the basal protein phosphorylation in microslices from different brain regions (hippocampus, cerebral cortex and cerebellum) of young rats fed a ketogenic diet, and we evaluated the effect of this diet on weight development and health of these rats based on serum biochemistry. Thirty-day-old rats consumed ad libitum ketogenic (high fat) or control diets for 8 wk. Rats consuming the high fat diet had ketonemia without signs of undernutrition or illness. Microslices were incubated in media containing (32)P-phosphate, and (32)P-phosphoprotein content was analyzed by one- or two-dimensional electrophoresis followed by autoradiography. Basal protein phosphorylation was greater in brain slices from ketogenic rats. Different increments of synapsin I, GAP-43 and GFAP phosphorylation were observed in two-dimensional autoradiography. A ketogenic diet induced metabolic changes affecting the basal status of protein phosphorylation. This change could affect the mechanisms of signal transduction in neural cells involved in the increase in the seizure threshold.

Animals↗