bluuebunny/crossref_metadata_2025_split huggingface dataset:
A STUDY OF PROPOSED DETERMINANTS OF BRAIN TRYPTOPHAN CONCENTRATION IN RATS AFTER PORTOCAVAL ANASTOMOSIS OR SHAM OPERATION
Authors: Bloxam D. L. , Curzon G. 
Published: October 2006

AbstractLiver dysfunction was produced in rats by surgical portocaval anastomosis (PCA), and the time‐course of changes in brain tryptophan and 5‐HT metabolism studied in relation to plasma changes possibly influencing brain tryptophan concentration.Brain tryptophan and 5‐hydroxyindolylacetic acid (5‐HIAA) levels were increased greatly and maximally on the day after PCA and remained high. 5‐HT changes were less marked but had a similar time‐course. Plasma total tryptophan was little changed but plasma free tryptophan was raised. The latter change showed a similar time‐course to that of brain tryptophan but was not large enough to account completely for it. Sham operation was followed by significant but transient increases in plasma free tryptophan, brain tryptophan and 5‐HIAA but these were much smaller than after PCA.Brain tryptophan did not correlate with plasma total tryptophan either in control or PCA rats but it correlated significantly with plasma free tryptophan in both groups. However brain levels were much higher in PCA rats than in controls with similar plasma free tryptophan levels at all times from the first day after operation. The increase of brain tryptophan in anastomosed rats not accounted for by plasma free tryptophan was explained neither by insulin changes nor by an increase of the insulin/glucagon ratio nor by changes in plasma concentrations of those amino acids which compete with tryptophan for entry into brain. The results therefore indicate an unknown influence on brain tryptophan concentration in PCA rats. As tyrosine changes in brain and plasma after PCA were very similar to those of tryptophan this influence may not be specific to tryptophan. Results suggest that under the conditions used brain tryptophan concentrations of both PCA and control rats are more influenced by changes of plasma free tryptophan concentration than by changes of plasma concentrations of competing amino acids.
DETERMINATION OF CATECHOLAMINES IN RAT BRAIN PARTS BY REVERSE‐PHASE ION‐PAIR LIQUID CHROMATOGRAPHY
Authors: Felice Lawrence J. , Felice Joan D. , Kissinger Peter T. 
Published: October 2006

Abstract—An improved method for the measurement of catecholamines in brain parts has been developed, based on reverse‐phase ion‐pair chromatography. The new method offers the advantages of high efficiency microparticulate liquid chromatography packings and the flexibility of ion‐pair chromatography. By this approach norepinephrine and dopamine (DA) have been measured in the hypothalamus and corpus striatum of the rat brain during various stages of development (15, 21, 30 days). Data are reported on the basis of the whole part and per weight of tissue. For the adult animals, the following concentrations (ng/g wet tissue) were observed for the hypothalamus: NE = 2261 ± 274, DA = 440 ± 103, and for the corpus striatum: DA = 11,888 ± 1840. The overall precision of the method was ±5.6% relative s.d. The absolute recovery was 60 ± 5% relative s.d. and was constant over the range of 1 ng to 1 μg of dopamine or norepinephrine per tissue sample. The relative retention behavior of 18 neurologically important catechol derivatives is reported for reverse‐phase chromatography with octyl sulfate as the stationary phase modifier.
MEASUREMENT OF PROTEIN TURNOVER IN RAT BRAIN1
Authors: Chee Po Yok , Dahl June L. 
Published: October 2006

Abstract— Degredation rates of rat brain proteins were measured by following the decay in specific radioactivity of carboxyl labelled aspartate and glutamate over a 17‐day period. Initial labelling of these amino acids was achieved by a single intraperitoneal injection 0f NaH14CO3. The non‐linear decay curve for total brain proteins could be approximated by assuming that the mixture contained two classes of proteins with half‐lives of 3.3 and 8.7 days, respectively. Half‐lives of 2.5 and 7.7 days were estimated for such protein classes in the microsomal fraction. The half‐lives of soluble proteins, synaptic membranes, cell body and synaptic mitochondria were 3.1, 5.8, 5.6 and 8.4 days, respectively. Identical results were obtained if the change in specific activity of intact protein labeled by NaH14CO3 was followed.Two‐fold slower decay rates were obtained when brain proteins were labeled with a pulse of [4,5‐3H]leucine or [l‐14C]leucine. Half‐lives calculated for the two classes of proteins in whole brain were 8.4 and 16.5 days, respectively with [4,5‐3H]leucine and 8.9 and 14.2 days, respectively with [1‐14C]leucine. These results indicate the very significant reutilization of this amino acid in brain. Sodium [14C]bicarbonate is a more satisfactory isotopic precursor for accurate assessment of rates of protein turnover in brain.
THE ROLE OF INTRANEURONAL 5‐HT AND OF TRYPTOPHAN HYDROXYLASE ACTIVATION IN THE CONTROL OF 5‐HT SYNTHESIS IN RAT BRAIN SLICES INCUBATED IN K+‐ENRICHED MEDIUM
Authors: Hamon M. , Bourgoin S. , Artaud F. , Glowinski J. 
Published: October 2006

Abstract— The incubation of brain stem slices from adult rats in a K+‐enriched medium containing a 5‐HT uptake inhibitor (fluoxetine) significantly increased their capacity to synthesize 5‐HT from tryptophan. The K+‐induced stimulation of 5‐HT synthesis was at least partly dependent on the depletion of the indoleamine in tissues since: (1) a good correlation was found between the respective changes in 5‐HT release and synthesis evoked by high K+ concentrations in the presence of various 5‐HT uptake inhibitors; (2) the modifications in endogenous 5‐HT levels produced by in vim treatments with drugs (reserpine, pargyline) or by incubating slices with 5‐HT altered the stimulating effect of high K+ concentrations and fluoxetine on 5‐HT synthesis; (3) the replacement of Ca2+ by Co2+ (4 mM) or EGTA (0.1 mM) in the incubating medium completely prevented the increased 5‐HT release and synthesis evoked by high K+ concentrations and fluoxetine.The extraction of tryptophan hydroxylase from incubated tissues revealed that the increased 5‐HT synthesis occurring in K+‐enriched medium was associated with an activation of this enzyme. Kinetic analyses indicated that this activation resulted from an increase in the Vmax of tryptophan hydroxylase, its apparent affinities for both tryptophan and 6‐MPH4 being not significantly affected. In contrast to the tryptophan hydroxylase from tissues incubated in normal physiological medium, the activated enzyme from tissues depolarized by K+ was hardly stimulated by Ca2+‐mediated phosphorylating conditions. This led to the proposition of a hypothetical model by which the Ca2+ influx produced by the neuronal depolarization would trigger the activity of a Ca2+‐dependent protein kinase capable of activating tryptophan hydroxylase. Although this sequence is still largely speculative it must be emphasized that, as expected from such a model, the regional differences in the K+‐evoked activation of tryptophan hydroxylase in slices (cerebral cortex > brain stem > spinal cord) were parallel to those of the Ca2+‐dependent protein phosphorylation (r= 0.92) and those of the activating effect of phosphorylating conditions on soluble tryptophan hydroxylase (r= 0.96).
ON THE ELIMINATION OF CENTRALLY FORMED 5‐HYDROXYINDOLEACETIC ACID BY CEREBROSPINAL FLUID AND URINE
Authors: Aizenstein Moacyr L. , Korf Jakob 
Published: October 2006

Abstract— In rats, the release of centrally formed 5‐hydroxyindoleacetic acid (5‐HIAA) into brain and spinal cord perfusates and urine was measured. Data from spinal cord perfusion of anaesthetized rats indicate that more than about 36% of the spinal production (122ng/h) of 5‐HIAA is eliminated via the cerebrospinal fluid (CSF). More than 30% of cerebrally formed 5‐HIAA (265.0 ng/h) was calculated to be released into ventricular‐cisternal perfusates. Of the total amount of 5‐HIAA found in the urine we estimated that about 8% originates in the central nervous system (CNS).In probenecid treated animals there was a substantial increase in the outflow of 5‐HIAA in both perfusion systems. In the combined perfusion experiments no proportional increase of the cerebral contribution to the cisternal outflow was found after probenecid. Our data indicate that a significant proportion of centrally formed 5‐HIAA is eliminated by the CSF. No evidence was found for an increased contribution of cerebral 5‐HIAA to lumbar CSF after application of the probenecid test. Urinary levels of 5‐HIAA do not reflect quantitatively central 5‐hydroxytryptamine metabolism.
PURIFICATION AND EFFECT OF THE NEUROTOXIN FROM THE SEA ANEMONE PARASICYONIS ACTINOSTOLOIDES
Authors: Ishikawa Y. , Onodera K. , Takeuchi A. 
Published: October 2006

Abstract— Three toxic components were isolated from the sea anemone, Parasicyonis actinostoloides. Among these components a main component had an effect on the neuromuscular transmission of the crayfish. The component was purified and found to be a basic polypeptide having a molecular weight of about 2000. Amplitudes of excitatory and inhibitory poslsynaptic potentials were increased by the toxin. It was found that the quantum content increased markedly in the excitatory synapse. The action of the toxin remained for a long time after the nerve–muscle preparation was thoroughly washed. These results suggest that the toxin has an effect on the presynaptic nerve.
Nerve Growth Factor: Biological Significance, Measurement and Distribution
Authors: Harper G. P. , Thoenen H. 
Published: October 2006

CONCLUSIONNGF proteins probably act as informational molecules transferred from end organs to the neurons of the sympathetic nervous system. The direct demonstration of the NGF content of most end organs requires assays more sensitive than those currently available. The high levels of NGF produced by some organs are probably of some other physiological significance.
Comparative Effects of Ethanol and Malnutrition on the Development of Catecholamine Neurons: Changes in Specific Activities of Enzymes
Authors: Detering Nancy , Edwards Elvira , Ozand Pinar , Karahasan Alp 
Published: October 2006

Abstract:A rat model was developed in which the comparative effects of malnutrition and ethanol on the neurochemical maturation of catecholamine neurons in brain were studied. The animals were offspring of rats optimally nourished (control pups), fed a diet with 35% of the calories supplied by ethanol (EtOH pups), or a diet calorically equivalent to the latter but lacking ethanol (isocaloric = IC pups). These latter two groups were calorically deprived since rats fed the diet containing ethanol ate 40–60% less than the optimally nourished group. The diets were administered to dams either during the last week of gestation (prenatal) or during lactation (postnatal). The protein content per gram wet weight was not significantly different between brains of control and experimental pups. Developmental changes in EtOH pups were noted in the activities of tyrosine hydroxylase (TOH) and dopamine β‐hydroxylase (DBH). The specific activity of TOH was increased in EtOH and IC pups preand postnatally. In the postnatal experimental group TOH activity in the brains of EtOH pups was higher not only when compared with control pups but also with IC pups. Prenatal caloric deprivation or ethanol exposure also caused increased specific activity of DBH in the neonatal rat brain. In contrast, exposure to ethanol postnatally caused a significant and persistent reduction in the specific activity of DBH, not only compared with control pups but also to matched IC pups exposed postnatally to the IC diet. The specific activity of 3,4‐dihydroxyphenylalaninedecarboxylase (DOPADC) was significantly elevated in the brains of prenatal and postnatal EtOH and IC pups, with little difference between the groups. Activities of monoamine oxidase (MAO) or catecholamine‐0‐methyltransferase (COMT) were generally lower in EtOH or IC pups than in control pups, again with little difference between EtOH and IC pups. These results suggest that an impaired metabolism of dopamine and norepinephrine is detectable in the brains of pups as a consequence of malnutrition, ethanol exposure, or both.
The Effect of Reducing Agents on the Apparent Molecular Weight of the Myelin P0 Protein and the Possible Identity of the P0 and “Y” Proteins
Authors: Cammer W. , Sirota S. R. , Norton W. T. 
Published: October 2006

Abstract:During sodium dodecyl sulfate polyacrylamide gel electrophoresis of sciatic nerve myelin proteins, the P0 protein migrated to two different positions on the gels. The distribution of P0 between the two forms depended on the concentration of mercaptoethanol (ME) or dithiothreitol (DTT) in the sample solvent. At >1% ME or 3.5% DTT, P0 was almost entirely in a form with an apparent molecular weight of 30,000, whereas in the absence of ME or DTT all the P0 migrated with an apparent molecular weight of 25,000. The distribution of the P0 protein between the two bands was independent of whether proteinase inhibitors were used during preparation of myelin. Furthermore, in a sample containing the more rapidly migrating form of P00, the P0 could be converted to the slower‐migrating form by addition of mercaptoethanol. These data show that interconversion of the two forms of P0 does not involve proteolytic degradation, but suggest rather that ME cleaves one or more intramolecular disulfide bonds in P0 unfolding the amino acid chain and thereby converting the form with a lower apparent molecular weight to that with a higher apparent molecular weight. We postulate that the “Y” protein band, which has been observed, in variable quantities, migrating slightly ahead of P0, may represent its oxidized form.
Interactions of GM1 Ganglioside with Crude Rat Brain Neuronal Membranes
Authors: Toffano G. , Benvegnù D. , Bonetti A. C. , Facci L. , Leon A. , Orlando P. , Ghidoni R. , Tettamanti G. 
Published: October 2006

Abstract:The binding of GM1, ganglioside to crude preparations of rat brain neuronal membranes was studied, the following results being obtained: (a) the binding process followed a biphasic kinetics, which displayed a break at 0.07–0.08 X 10−6m GM1, concentration; (b) the features of the binding process at GM1, concentrations below the break and, over the break, above 10‐6m appeared to be different. Below the break the process proceeded slowly and brought a stable and irreversible association of GM1, molecules to the membranes. Over 10‐6m the process was much more rapid and caused GM1, molecules to interact in such a way that they were releasable by washing and could exchange with newly added free ganglioside; (c) the two binding processes displayed the characteristics of a saturation phenomenon; (d) in both cases, GM1, taken up was freely available to galactose oxidase, indicating that the oligosaccharide chains protrude from the membrane surface. We postulate that GM1, occurs, below and above the break, in different physical forms, each of them having a different mechanism of interaction with the membrane. Above 10‐6m GM1, interacts as micelles, and the basis of the micelle‐membrane inter action is a fusion process. Below the break, in the 10−8–10−7m range, the binding is the result of hydrophobic interactions between sites on the membrane and the hydrophobic portion of individual ganglioside molecules, most likely in the monomeric form. Toffano G. et al. Interactions of GM1, ganglioside with crude rat brain neuronal membranes. J. Neurochem.35, 861–866 (1980).
Neopterin and Biopterin Levels in Patients with Atypical Forms of Phenylketonuria
Authors: Nixon Jon C. , Lee Ching‐Lun , Milstien† Sheldon , Kaufman Seymour , Bartholomé Klaus 
Published: October 2006

Abstract:The pattern of unconjugated pterins in liver tissue and in urine from patients with atypical forms of phenylketonuria with hyperphenylalaninemia (HPA) has been investigated with a high performance liquid chromatographic technique. Two patients with defects in the biosynthesis of biopterin have been shown to have higher than normal levels of neopterin and lower than normal levels of biopterin. In contrast, a patient with HPA due to a deficiency of dihydropteridine reductase has the reverse urinary pattern, i.e., high biopterin, low neopterin. These results indicate that the ratio of neopterin to biopterin in urine can be of value in discriminating between HPA due to a deficiency of phenylalanine hydroxylase (classic PKU), HPA due to dihydropteridine reductase deficiency, and HPA due to a block in the biosynthesis of biopterin.
Differential Changes in Monoamine Oxidase A and B Activity in the Aging Rat Brain
Authors: Benedetti M. Strolin , Keane P. E. 
Published: October 2006

Abstract:The activity of monoamine oxidase (MAO) was assayed in the brains of young adult (7–8 weeks old) and aging (95–104 weeks old) male Sprague‐Dawley rats. When expressed per milligramme of tissue, total protein content was increased to a similar extent in whole brain and in all seven brain regions of the aging rat, whereas MAO A activity (assayed by using 5‐hydroxytryptamine as substrate) was unchanged in whole brain but increased in the cerebellum, and fell in the brainstem, midbrain, hippocampus, and cortex; and MAO B activity (assayed by using β‐phenylethylamine as substrate) increased in whole brain and all regions, except the brainstem. Age‐related changes in total protein, MAO A, and MAO B were thus independent of each other. Kinetic studies indicated that the Vmax of MAO B was increased in aging rat brain, whereas the Km was unaltered. The increase in MAO B activity was restricted to the extrasynaptosomal mitochondrial fraction of the aging brain, whereas a reduction in MAO A activity was found in the intrasynaptosomal, but not the extrasynaptosomal mitochondrial fraction.
Nature of the Autofluorescent Material in Cerebrocortical Necrosis
Authors: Edwin E. E. , Jackman R. 
Published: October 2006

Abstract:A distinctive autofluorescence under ultraviolet light has been observed in the cerebral cortex of young ruminants suffering from cerebrocortical necrosis. The fluorescence is intimately connected with structural elements of the brain and cannot be extracted into solvents by normal procedures. The work presented here shows it to be associated with a collagen‐like material.
Glucose Availability to Individual Cerebral Structures Is Correlated to Glucose Metabolism
Authors: Hawkins Richard A. , Mans Anke M. , Davis Donald W. , Hibbard Lyndon S. , Lu Daniel M. 
Published: October 2006

Abstract:Regional cerebral glucose influx was measured using quantitative autoradiography after the intravenous infusion of [2‐14C]glucose for a period of 10 or 20 s. Glucose influx varied considerably among structures over an almost threefold range. When compared with rates of regional glucose utilization, a significant correlation by region was found between glucose influx and utilization, demonstrating that the glucose supply to individual cere bral structures is closely matched to their metabolic needs.
Regulation and Properties of an NADP+ Oxidoreductase Which Functions as a γ‐Hydroxybutyrate Dehydrogenase
Authors: Kaufman E. E. , Relkin N. , Nelson T. 
Published: October 2006

Abstract:A number of naturally occurring biological intermediates have been found to inhibit competitively the activity of a highly purified NADP+‐dependent oxidore‐ductase which catalyzes the simultaneous oxidation of γ‐hydroxybutyrate to succinic semialdehyde, and the reduction of D‐glucuronate to L‐gulonate. Of the inhibitors studied, those with the lowest Ki are the α‐keto analogues of the branched chain or aromatic amino acids. The Vmax and Km for this enzyme are affected by pH; consequently, changes in substrate concentration can markedly alter the pH optimum. The enzyme has been found to be inhibited by reducing agents such as dithiothreitol and mercapto‐ethanol, protected against this inhibition by oxidizing agents such as oxidized glutathione or H2O2, and finally, protected against heat inactivation by the presence of either NADP+ or NADPH.
Effect of Maternal Iron Deficiency in Rat on Serotonin Uptake In Vitro by Brain Synaptic Vesicles in the Offspring
Authors: Kaladhar M. , Rao B. S. Narasinga 
Published: October 2006

Abstract:The effect of maternal dietary iron deficiency on brain synaptic vesicle [3H]serotonin (5‐HT) uptake and iron content in the offspring was examined in rats. Pups born to iron‐deficient mothers revealed significant deficits in vesicular [3H]5‐HT uptake and iron concentration at 21 days of age. These changes were, however, found to be reversible with postweaning iron repletion.
Effect of Ethylcholine Mustard on Choline Dehydrogenase and Other Enzymes of Choline Metabolism
Authors: Barlow P. , Marchbanks R. M. 
Published: October 2006

AbstractThe effect of ethyl choline mustard (ECMA), an effective irreversible inhibitor of choline transport, was investigated on the enzymes of choline metabolism. ECMA at concentrations of 50 μM hardly affected choline acetyltransferase and caused only a 20% inhibition of choline kinase at a concentration of 1 mM. However, the mustard was an extremely effective inhibitor of choline dehydrogenase, producing 50% inhibition at concentrations of 6 μM. The inhibition was prevented by incubation in the presence of choline or by prior reaction of the mustard with thiosulphate. Separation of the components of the ECMA solution on TLC suggested that only the compound with an aziridine ring was an effective inhibitor of choline dehydrogenase. The inhibition was resistant to the washing out of excess unreacted mustard. The rate constant of inhibition was 395 M'‐1 s‐1. By the use of [3H]ECMA a single polypeptide in the enzyme preparation having a MW of 67,000 was labelled. The labelling was thiosulphate‐sensitive and prevented by incubation with choline. It is concluded that ECMA is an irreversible inhibitor of choline dehydrogenase. It is at least as effective an inhibitor of choline dehydrogenase as of the choline transport system, although it does not appreciably inhibit choline acetyltransferase or choline kinase in the micromolar range.
Nicotinic Stimulation of [3H]Acetylcholine Release from Mouse Cerebral Cortical Synaptosomes
Authors: Rowell Peter P. , Winkler Donald L. 
Published: October 2006

AbstractThe effects of nicotine and 1,1‐dimethyl‐4‐phenylpiperazinium (DMPP) on the release of newly synthesized [3H]acetylcholine in mouse cerebral cortical synaptosomes were examined. Nicotine and DMPP produced increases in [3H]acetylcholine release, over the level of spontaneous release, of 24% and 30%, respectively, of a maximum depolarization‐induced release produced by 50 mM potassium. The maximum effect was achieved at a concentration of 1 × 10‐4M for both agents. The time course of release indicated a slow onset of action, reaching a maximum effect at 15 min of incubation. Both nicotine and DMPP also produced a slightly greater release of total tritium, measured in the absence of cholinesterase inhibition, than of [3H]acetylcholine. The release induced by nicotine was completely antagonized by hexamethonium and was largely (58%) calciumdependent. Nicotine also produced an increase in [3H]choline accumulation into synaptosomes. These results indicate that the nicotinic agonists nicotine and DMPP can produce a moderate enhancement of acetylcholine release by a receptor‐mediated action on cholinergic nerve terminals in the central nervous system.