bluuebunny/crossref_metadata_2025_split huggingface dataset:
SYNTHESIS OF RNA IN DEVELOPING RAT BRAIN IN VITRO
Authors: Sharma Shail K. , Singh U. N. 
Published: October 2006

Abstract—Incorporation of [8‐14C]adenine into a rapidly‐labelled fraction of RNA derived from the nucleus, and into a cytoplasmic RNA of high molecular weight was studied in brain slices from new born rats. The kinetic behaviour of the two fractions of RNA was compatible with a precursor‐product relationship between them. The change in the specific activity of adenine and the reduction of radioactivity in prelabelled RNA of brain slices in the presence of actinomycin D, suggest that the observed degradation of nuclear RNA is not due to random changes, but is limited to a relatively small fraction, presumably messenger RNA.
ADENOSINETRIPHOSPHATASE AND NUCLEOTIDE METABOLISM IN SYNAPTOSOMES OF RAT BRAIN1
Authors: Abdel‐Latif Ata A. , Smith Jack P. , Hedrick Nina 
Published: October 2006

Abstract—In the presence of synaptosomes prepared from rat brain, only ATP, dATP and ADP but not dADP were active as substrates of phosphatase (ATP phosphohydrolase; EC 3.6.1 4) in the presence of 150mm‐Na+ and 20mm‐K+. An active adenylate kinase (ATP:AMP phosphotransferase; EC 2.7.4.3.) was demonstrated in the synaptosomal fractions by means of paper chromatography, paper electrophoresis and enzymic reactions, so that the high activity with ADP as substrate could represent an activity of an ATPase. Apparently dADP was not a substrate for the kinase; no dATP was formed when dADP was incubated with the synaptosomal fraction in the presence of Na+, K+ and Mg2+. Small amounts of P1 were liberated with dADP, IDP, GDP or CDP, but not UDP, as substrates, but none was produced in the presence of mononucleotides. The adenine‐deoxyribose bond, but not the adenine‐ribose bond, was hydrolysed upon the addition of 5% (w/v) TCA to the reaction mixture.The KM for the hydrolysis of ATP but not ITP, in the presence of Mg2+, or of Na+, K+ and Mg2+, was lower for the synaptosomal ATPase than for the microsomal ATPase, and the values for Vmax for synaptosomal ATPase were higher. The activation increment was generally higher for the synaptosomal ATPase and no distinct differences in the properties of the enzyme from either particulate fractions were observed. Mg2+ could be partially replaced by Mn2+ in the synaptosomal ATPase system, but there was little Na+‐K+‐activation observed in the presence of the latter. The effects of ouabain and of homogenization under various conditions suggested localization of the K+‐sensitive site of the ATPase on the surface of the synaptosomal membrane. Activity of the Na+‐K+‐Mg2+ ATPase increased after freezing and thawing of the sonicated, sucrose or tris‐treated preparations but decreased considerably in the synaptosomes treated with 001 m‐deoxycholate. Activity of the Mg2+ ATPase in the latter preparation showed little change.
LEVELS OF AMINO ACIDS AND PROTEINS IN PACINIAN CORPUSCLES OF THE CAT
Authors: Santini M. , Berl S. 
Published: October 2006

Abstract— Paper chromatography of extracts from mesenteric Pacinian corpuscles of the cat revealed the presence of glutamic acid, glutamine, aspartic acid and alanine as major amino acids, and glycine, serine and threonine in traces; GABA was not detected. Levels of glutamic acid (0·75 μmol/g ′ 0·37, s.d.), glutamine (1·34 ± 0·55), and aspartic acid (0·32 ± 0·22) of mesenteric and pancreatic samples of Pacinian corpuscles were determined by separation on chromatographic columns. The protein values averaged 5·2 ± 0·66 per cant of the wet weight.Treatment of the cats with reserpine or pargyline or deafferentation of the Pacinian corpuscles did not significantly alter these values.
TRYPTOPHAN TRANSPORT ACROSS THE SYNAPTOSOMAL MEMBRANE1
Authors: Grahame‐Smith D. G. , Parfitt A. G. 
Published: October 2006

Abstract—Crude mitochondrial fractions prepared from rat brains took up l‐tryptophan. The component of the crude mitochondrial fraction responsible for this uptake is the synaptosome. After uptake of tryptophan occurred, rupture of synaptosomes released 97 per cent of the tryptophan unchanged. Rupture of synaptosomes abolished uptake.Penetration of the limiting membrane of synaptosomes by l‐tryptophan both as influx and efflux was studied. Uptake of l‐tryptophan was rapid, temperature dependent, partially inhibited by cyanide, 2‐deoxy‐d‐glucose and ouabain, but apparently unaffected by low external sodium ion concentrations. d‐tryptophan was a poor inhibiteur of l‐tryptophan uptake. Concentration gradients Internal: external of up to 4:1 were achieved. Kinetic studies on l‐tryptophan uptake and its competitive inhibition by l‐phenylalanine indicated a saturable carrier‐mediated transport system, present in the rat at birth. l‐Tryptophan efflux from preloaded synaptosomes was markedly stimulated by certain arrino acids and its influx stimulated by preloading with l‐tryptophan. This countertransport is further evidence for carrier‐mediated or facilitated diffusion. On the basis of countertransport data there seem to be at least two systems for transporting amino acids across synaptosomal membrane.The relevance of these studies to the role of l‐tryptophan as the initial precursor of brain 5‐hydroxytryptamine is examined.
THE ACTIVITY OF GANGLIOSIDE SIALIDASE IN THE DEVELOPING HUMAN BRAIN
Authors: ÖHman R. , Svennerholm L. 
Published: October 2006

Abstract—The development of ganglioside sialidase and of four different p‐nitrophenyl glycosidases in human brain was investigated including both prenatal and postnatal periods. The developmental curve for sialidase was different from that of the other glycosidases. While p‐nitrophenyl glycosidases showed high activities at an early stage of development (21 foetal weeks), and remained at about the same level, ganglioside sialidase was not detected before the foetal age of 15‐20 weeks. The sialidase activity at term reached about half the adult level and there was a possible decrease in activity during the first year. The sialidase activity then increased, approaching the adult level at about the age of 5 years. The development of the ganglioside sialidase activity in human brain can be related to changes in the concentration of individual brain ganglioside components. The late maturation of the sialidase system in relation to other glycohydrolases is also discussed as a possible protective mechanism for sialic acid‐containing compounds during the early period of development.
INCORPORATION OF [14C]N‐ACETYL NEURAMINIC ACID INTO BRAIN GLYCOPROTEINS AND GANGLIOSIDES IN VIVO1
Authors: De Vries G. H. , Barondes S. H. 
Published: October 2006

Abstract—Intracerebrally administered [14C]N‐acetyl neuraminic acid was incorporated into brain glycoproteins and gangliosides. Incorporation into both classes of compounds was markedly inhibited by acetoxycycloheximide but incorporation into the soluble glycoproteins of the nerve‐ending fraction was inhibited least of all. In contrast to glucosamine and fucose, a relatively small proportion of the injected [14C]NANA was incorporated.
CATECHOLAMINE METABOLISM IN THE DOG: COMPARISON OF INTRAVENOUSLY AND INTRAVENTRICULARLY ADMINISTERED [14C]DOPAMINE AND [3H]NOREPINEPHRINE
Authors: Chase T. N. , Breese G. R. , Gordon Edna K. , Kopin I. J. 
Published: October 2006

Abstract—The urinary excretion of labelled metabolites was measured in dogs which had been injected intravenously or intraventricularly with [3H]norepinephrine or [14C]dopamine. [3H]Norepinephrine injected by either route produced more labelled 3‐methoxy‐4‐hydroxy‐phenylglycol than 3‐methoxy‐4‐hydroxymandelic acid, as did [14C]dopamine after intravenous administration. In contrast, following the intraventricular injection of [14C]dopamine, more [14C]3‐methoxy‐4‐hydroxymandelic acid was formed than [14C]3‐methoxy‐4‐hydroxyphenylglycol. These observations suggest that the metabolism of exogenously‐administered and endogenously‐formed norepinephrine may proceed through different routes and that the predominant metabolite of norepinephrine in canine brain may be 3‐methoxy‐4‐hydroxymandelic acid rather than 3‐methoxy‐4‐hydroxyphenylglycol.
ABSENCE OF DIRECT ACTION OF INSULIN ON METABOLISM OF THE ISOLATED PERFUSED RAT BRAIN1
Authors: Sloviter H. A. , Yamada H. 
Published: October 2006

AbstractThe ability of insulin to influence directly the metabolism of the mammalian brain has been evaluated with an isolated, perfused rat brain preparation. Insulin was added to the perfusion fluid or was injected into the rat from which the isolated brain preparation was subsequently made. The spontaneous electrical activity of the brain, the rate of cerebral glucose consumption and the rate of efflux of K+from the brain were not affected by insulin. We conclude that insulin either does not act directly on the brain or that its action is very small and/or very slow in comparison with its action on other tissues. We suggest that the effects on brain metabolism reported to occur after administering insulin and glucose to the intact animal may be secondary to the large stimulation of the metabolism of the liver and/or other organs.
ENHANCED FRAGILITY OF NEURAL LYSOSOMES FROM CHICKS SUFFERING FROM GALACTOSE TOXICITY1
Authors: Blosser J. C. , Wells W. W. 
Published: October 2006

Abstract—The stability of neural lysosomes to osmotic and temperature shock and the free (non‐sedimentable) activities of selected lysosomal hydrolases from chicks suffering from galactose neurotoxicity were investigated. The neural lysosomes from chicks fed galactose demonstrated enhanced fragility to both elevated temperature and hypo‐osmotic media in comparison to the behavior of neural lysosomes isolated from control animals. The increased lability to osmotic shock could be duplicated by preincubation of normal lysosomes in solutions of galactose or galactitol. Further, the increased fragility induced in vivo by galactose feeding could be reversed by removing the chicks from the diet for 8 h, and such removal was accompanied in the brain by large reductions in levels of galactose and galactitol. The free activities of both β‐galactosidase (EC 3.2.1.23) and β‐N‐acetyl hexosaminidase (EC 3.2.1.30) were elevated above those of controls, and the percentage increases were proportional to the combined brain levels of galactose and galactitol. Our data suggest that increased fragility of lysosomes is a function of the accumulation of galactose and galactitol in the brains of chicks fed toxic amounts of galactose. Alteration of lysosomal integrity represents an attractive role for galactitol, as well as galactose, in the causation of galactose neurotoxicity in chicks.
ENZYME HISTOCHEMISTRY OF THE RAT HYPOTHALAMUS DURING EARLY DEVELOPMENT
Authors: Robinson N. 
Published: October 2006

Abstract—The distribution, localization and changes in intensity of enzymes in major metabolic pathways of brain metabolism during the first 16 days postnatal life of the rat anterior hypothalamus are reported. Thiamine pyrophosphatase, acid phosphatase and 5′‐nucleotidase showed rapid increases in activity between 0 and 5 days whilst AChE, Mg2+–ATPase and monoamine oxidase exhibited little or no activity before 3 days. Most enzymes showed a moderate intensity at 16 days in all nuclei whilst for some enzymes of phosphate metabolism the reaction was strong. The precocity of some enzymes particularly monoamine oxidase, lactate dehydrogenase and NADH2‐diaphorase seen in other regions at birth, was not apparent in hypothalamic nuclei. Comparisons are made with other regions of the brain and the findings discussed in relation to function.
ENDOGENOUS MICROSOMAL PHOSPHOLIPID PEROXIDATION IN MOUSE BRAIN
Authors: Konat G. 
Published: October 2006

Abstract— Release of malondialdehyde from microsomal phospholipids during incubation in vitro was studied in the brain cytoplasm and in the microsomes fortified by deproteinized cytosole.Linearity between the log of specific activity of peroxidation (malondialdehyde release) and the negative log of protein concentration was demonstrated. The boiling of microsomes significantly quenched the ability to produce malondialdehyde, while preincubation with phospholipase A completely abolished this ability.In general, aromatic and not aliphatic compounds inhibited the reaction. 1,1,1‐Trichloro‐2,2‐bis (p‐chlorophenyl) ethane (DDT) was found to be a selective inhibitor of membrane peroxidative activity. The maximal inhibition is invariable. The data obtained revealed that brain and liver microsomal phospholipid peroxidation differ in some respects and the differences are of both quantitative and qualitative nature.
SYNTHESIS OF ACETYLCHOLINE IN DIFFERENT COMPARTMENTS OF BRAIN NERVE TERMINALS IN VIVO AS STUDIED BY THE INCORPORATION OF CHOLINE FROM PLASMA AND THE EFFECT OF PENTOBARBITAL ON THIS PROCESS
Authors: Aquilonius S.‐M. , Flentge F. , Schuberth J. , Sparf B. , Sundwall A. 
Published: October 2006

AbstractThe time course of the incorporation of choline from plasma into a high and a low molecular weight fraction from mouse brain synaptosomes was studied. The fractions were obtained from lysed synaptosomes by gel filtration on Sephadex G‐25. An extremely rapid incorporation of radioactivity into acetylcholine was found in both fractions and in the time interval 0.25‐9 min after the intravenous administration of labelled choline, higher specific radioactivities of acetylcholine were found in the high molecular weight fraction than in the low molecular weight fraction. However, the specific radioactivity of choline in the high molecular weight fraction was much lower than that of acetylcholine. It was found that barbiturate anaesthesia caused a marked decrease in the labelling of acetylcholine in the high molecular weight fraction while the incorporation into the low molecular weight fraction was affected to a much smaller extent.Acetylcholine of the high molecular weight fraction showed properties similar to those of vesicle‐bound acetylcholine.The recoveries of labelled and endogenous acetylcholine and choline from the brain homogenates were calculated in different steps of the fractionation procedure. In the fraction containing lysed synaptosomes the recovery of radioactive acetylcholine was lower than that of endogenous acetylcholine. This may indicate the presence of two types of bound acetylcholine in the synaptosomes.Different models for the intraneuronal synthesis of acetylcholine are discussed and it is proposed that a site of acetylcholine synthesis in vivo may be closely associated with some constituent of the high molecular weight fraction and directly coupled with the storage of the transmitter.
DEVELOPMENT OF THE BLOOD‐BRAIN BARRIER FOR 6‐HYDROXYDOPAMINE
Authors: Sachs Charlotte 
Published: October 2006

AbstractThe postnatal development of the blood‐brain barrier for the neurotoxic action of 6‐hydroxydopamine on central noradrenaline neurons has been investigated by recording the in vitro uptake of [3H]noradrenaline in slices from cerebral cortex, hypothalamus and spinal cord in rats treated with large doses of 6‐hydroxydopamine at different ages. The [3H]noradranaline uptake was permanently and markedly reduced in all regions when the animals were treated at birth, certainly related to degeneration of noradrenaline neurons, caused by 6‐OH‐DA. In the cerebral cortex and hypothalamus an efficient protection against the effects of 6‐OH‐DA on [3H]noradrenaline uptake developed postnatally, while in the spinal cord this protection was never seen to become complete. The results obtained indicate a rapid formation of a blood‐brain barrier for 6‐OH‐DA in the cerebral cortex between the 7th and 9th day after birth. In the hypothalamus the development of this barrier seemed to have a more gradual time‐course, but appeared to be fully developed already at day 5 postnatally. Also in the spinal cord the barrier developed more gradually from birth to the adult age. It was observed, however, that both in the cerebral cortex and in the spinal cord, the blood‐brain barrier developed, could not completely protect the central noradrenaline neurons from the neurotoxic actions of large doses of 6‐OH‐DA administered systemically to adult rats. Furthermore, the results obtained support the view that 6‐OH‐DA does not seem to apparently affect the outgrowth of remaining NA neurons which have not been destroyed by the 6‐OH‐DA treatment.
AMINO ACIDS IN SYNAPTIC VESICLES FROM MAMMALIAN CEREBRAL CORTEX: A REAPPRAISAL
Authors: De Belleroche J. S. , Bradford H. F. 
Published: October 2006

AbstractSynaptic vesicles were prepared from rat cerebral cortex and separated by gel filtration from small molecular weight compounds contaminating this fraction. Electron microscopy of the vesicle suspension showed that vesicles were by far the most abundant morphological entities. The amino acid content of the purified vesicle fraction was examined and the two amino acids appearing in the most significant amounts were found to be taurine and glutamate. This amino acid pool was not osmotically sensitive as is the vesicular pool of ACh and remained attached to the vesicular protein after passage through Sephadex columns equilibrated in water. However, amino acids added to the vesicle fraction prior to passage through Sephadex did not become associated with this pool and this indicated that the vesicular pool was not likely to be an artifact due to the vesicular protein non‐specifically adsorbing amino acids. The release of taurine from incubated synaptosome beds was studied and elevated medium K+ (56 mm) was found to cause a small increase (36 per cent) in the amount of the taurine released to the medium. During the same experiments another physiologically active amino acid, glutamate, was released in more significant amounts, increasing in the medium by 186 per cent. The possible significance of the presence of taurine is discussed.
HIGH AFFINITY TRANSPORT OF CHOLINE INTO SYNAPTOSOMES OF RAT BRAIN1
Authors: Yamamura H. I. , Snyder S. H. 
Published: October 2006

Abstract—The accumulation of [3H]choline into synaptosome‐enriched homogenates of rat corpus striatum, cerebral cortex and cerebellum was studied at [3H]choline concentrations varying from 0.5 to 100 μm. The accumulation of [3H]choline in these brain regions was saturable. Kinetic analysis of the accumulation of the radiolabel was performed by double‐reciprocal plots and by least squares iterative fitting of a substrate‐velocity curve to the data. With both of these techniques, the data were best satisfied by two transport components, a high affinity uptake system with Km. values of 1.4 μM (corpus striatum), and 3.1 μM (ceμ(cerebral cortex) and a low affinity uptake system with respective Km. values of 93 and 33 μM for these two brain regions. In the cerebellum choline was accumulated only by the low affinity system. When striatal homogenates were fractionated further into synaptosomes and mitochondria and incubated with varying concentrations of [3H]choline, the high affinity component of choline uptake was localized to the synaptosomal fraction. The high affinity uptake system required sodium, was sensitive to various metabolic inhibitors and was associated with considerable formation of [3H]acetylcholine. The low affinity uptake system was much less dependent on sodium, and was not associated with a marked degree of [3H]acetylcholine formation. Hemicholinium‐3 and acetylcholine were potent inhibitors of the high affinity uptake system. A variety of evidence suggests that the high affinity transport represents a selective accumulation of choline by cholinergic neurons, while the low affinity uptake system has some less specific function.
ENZYMES CATALYZING THE DE NOVO SYNTHESIS OF METHYL GROUPS IN THE BRAIN AND OTHER TISSUES OF THE RAT
Authors: Ordóñez L. A. , Wurtman R. J. 
Published: October 2006

Abstract—Rat brain contains all three of the enzymes required for de novo synthesis of the methyl group of methionine (serine transhydroxymethylase, methylene reductase, and [B12]transmethylase) in activities comparable to those found in liver and kidney. The activities of methylene reductase in female kidney, and of [B12]transmethylase in female brain and kidney, are higher than in the corresponding male tissues. Liver and kidney extracts contain an inhibitor of methylene reductase not present in brain extracts. This inhibitor differs from S‐adenosylmethionine (SAM), which also inhibits methylene reductase in both liver and brain homogenates. The administration of l‐DOPA to rats, which has been previously shown to deplete brain S‐adenosylmethionine, also reduces the activity of brain [B12]transmethylase if assayed without added SAM. Since SAM is required for activity of this enzyme, its decreased activity probably results from the decline in brain SAM concentration. De now synthesis of methyl groups could be a mechanism by which the brain maintains its level of methionine in the face of increased methyl group utilization after administration of l‐DOPA.
METABOLISME DU CALCIUM ET LIBERATION DE L'ACETYLCHOLINE DANS L'ORGANE ELECTRIQUE DE LA TORPILLE
Authors: Babel‐Guérin Eliane 
Published: October 2006

Résumé—Le métabolisme du'calcium a étéétudié dans l'organe électrique de la Torpille, au repos et en activité, in vivo et in vitro, en mesurant le calcium total et en utilisant du 45Ca. Lorsque le tissu est mis en présence de fortes concentrations de calcium, un échange complet s'effectue entre le calcium cellulaire et celui du milieu d'incubation. En présence de faibles concentrations, le tissu retient son calcium qui, dans ce cas, séchange mal avec l'extérieur. La stimulation cause une augmentation nette du calcium cellulaire et accélère son échange avec le milieu extérieur. Cette entrée de calcium concerne principalement les terminaisons nerveuses présynaptiques car on l'observe aussi lorsque la transmission est bloquée par le curare qui agit au niveaja des électroplaques. Il semble que le calcium influence la répartition intracellulaire du transmetteur. En effet, l'entrée présynaptique de calcium s'accompagne d'une diminution de l'ACh ‘liée’ (vésiculaire). Lorsque le tissu est incubé dans une solution exempte de calcium, surtout en présence d'EDTA, la réponse électrophysiologique disparaît; le taux d'ACh ‘libre’ (disponible) diminue alors, mais son ‘turnover’ augmente. Le calcium extracellulaire est donc nécessaire au maintien du compartiment d'ACh immédiatement disponible.
THE INCORPORATION OF GLUCOSE INTO BRAIN GLYCOGEN AND THE ACTIVITIES OF CEREBRAL GLYCOGEN PHOSPHORYLASE AND SYNTHETASE: SOME EFFECTS OF AMPHETAMINE
Authors: Nahorski S. R. , Rogers K. J. 
Published: October 2006

Abstract— The effects of amphetamine sulphate (5 mg/kg intraperitoneally) on the incorporation of radioactive carbon from [U‐14C]glucose into the glycogen of mouse cerebral cortex, midbrain and hind‐brain have been investigated. In all brain regions studied amphetamine induced a rapid decrease in glycogen followed by a slower return to control values. No significant alterations were observed in the steady state concentration of cerebral glucose. The initial fall in glycogen was associated with a fall in its specific radioactivity relative to that of cerebral glucose, whereas the resynthesis of the polysaccharide was associated with a marked increase in the relative specific radioactivity of glycogen. Other experiments demonstrated that amphetamine initially stimulates the breakdown of prelabelled glycogen and that the resulting molecule has fewer 1,4 linked glucose side chains.Studies of the relative forms of the enzymes glycogen phosphorylase and glycogen synthetase suggested that rapid post mortem changes were less likely to occur if cerebral tissue was fixed by means of a freeze‐blowing technique. Amphetamine administration resulted in a rapid though transient elevation of phosphorylase a activity in mouse forebrain. The level of glycogen synthetase I activity was unchanged initially but was markedly elevated during the period when there was a large increase in the rate of incorporation of glucose into glycogen. It is suggested that cerebral glycogen metabolism is controlled, at least in part, by the interconversion of the ‘active’ and ‘inactive’ forms of glycogen phosphorylase and synthetase.