bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE EFFECTS OF OXYGEN DEPRIVATION ON ELECTRICALLY STIMULATED CEREBRAL CORTEX SLICES
Authors: SWANSON P. D. 
Published: October 2006

Abstract— (1) Thin slices were prepared from guinea pig cerebral cortex and allowed to incubate in oxygenated bicarbonate‐buffered medium for 30 min. Subsequent to that time the slices were made hypoxic by passing 95% N2‐5% CO2 through the medium. Hypoxic exposure caused the slices to gain Na+ and to lose K+ ions from the non‐inulin space. These shifts were especially pronounced when slices were electrically stimulated during the hypoxic period. Thus, after 30 min of hypoxia plus stimulation, non‐inulin Na+ had risen from 30 to 84, μequiv./g wet wt., and non‐inulin K+ had fallen from 50·5 to 14·3 μequiv./g wet wt.(2) The above shifts were in part reversible, but when reoxygenated slices were subsequently electrically stimulated in oxygenated media, they failed to lose K+ or to gain Na+.(3) The induced inexcitable state could not be attributed to inability of the slices to replenish ATP and phosphocreatine and may indicate an alteration in membrane constituents necessary for preservation of membrane excitability.
DISTRIBUTION OF AMINO ACIDS AND OF EXO‐ AND ENDOPEPTIDASES ALONG VERTEBRATE AND INVERTEBRATE NERVES
Authors: Marks N , Datta R. K , Lajtha A 
Published: October 2006

Abstract— The proximo‐distal gradients for representative peptidases, peptidylpeptide hydrolases, and amino acids were measured in segments of peripheral nerve from invertebrates and vertebrates and in the lobster brain and ventral cord.Crustacean nerve was characterized by a large pool of free amino acids totaling 100–200 μmoles/g wet wt. In lobster nerve, the principal free amino acid was aspartic acid which comprised 55 per cent of the free pool, whereas in the rat sciatic nerve it comprised only 5 per cent. The principal free amino acid in rat sciatic nerve was taurine (32 per cent of the pool) and in lobster brain glycine comprised 30 per cent of the pool. No consistent patterns emerged for the gradients along the nerves for amino acids and hydrolytic enzymes. In the leg nerve of the lobster, concentrations of aspartic acid and arginine were higher in the proximal region, and concentrations of proline and alanine were higher in the distal region. Concentrations of most amino acids were higher in the proximal regions of crab nerve, of lobster brain and ventral cord, and of rat sciatic nerve.Rat sciatic nerve exhibited a pronounced proximo‐distal increase in activity of aminopeptidase (Leu‐Gly‐Gly). In lobster leg nerve, activity of neutral proteinase was higher in the proximal segment, whereas activity of acid proteinase was higher in the distal segment. The best examples of proximo‐distal gradients were found in lobster brain and ventral cord; activities of endopeptidases, arylamidases (Leu‐ and Arg‐βNA), and aminopeptidase were higher in the supra‐esophageal ganglia or cephalothorax segments than in the distal regions.
EFFECTS OF 6‐HYDROXYDOPAMINE ON CATECHOLAMINE CONTAINING NEURONES IN THE RAT BRAIN
Authors: Uretsky N. J. , Iversen L. L. 
Published: October 2006

AbstractAfter the intraventricular injection of 6‐hydroxydopamine (6‐OHDA), there was a long lasting reduction in the brain concentrations of noradrenaline (NA) and dopamine (DA). The brain concentration of NA was affected by lower doses of 6‐OHDA than were required to deplete DA. A high dose of 6‐OHDA which depleted the brain of NA and DA by 81 per cent and 66 per cent respectively, had no significant effect on brain concentrations of 5‐hydroxytryptamine (5‐HT) or γ‐aminobutyric acid (GABA). The fall in catecholamines was accompanied by a long lasting reduction in the activities of tyrosine hydroxylase and DOPA decarboxylase in the hypothalamus and striatum, areas in the brain which are rich in catecholamine containing nerve endings. There was, however, no consistent effect on catechol‐O‐methyl transferase or monamine oxidase activity in these brain regions. The initial accumulation of [3H]NA into slices of the hypothalamus and striatum was markedly reduced 22–30 days after 6‐OHDA treatment. These results are consistent with the evidence in the peripheral sympathetic nervous system that 6‐OHDA causes a selective destruction of adrenergic nerve endings and suggest that this compound may have a similar destructive effect on catecholamine neurones in the CNS.
MANIFESTATION OF METABOLIC COMPARTMENTATION DURING THE MATURATION OF THE RAT BRAIN
Authors: Patel A. J. , Balázs R. 
Published: October 2006

Abstract—(1) The fate of [U‐14C]leucine was studied in rat brain in vivo from birth to five weeks of age. The major route of leucine metabolism at all ages was conversion into protein. The rate of protein synthesis was low in the newborn; it reached a peak at about 15 days and slowed down moderately later. Incorporation into brain lipids was relatively low under the experimental conditions (less than 2 per cent of the total tissue 14C).(2) The conversion of leucine‐carbon into amino acids associated with the tricarboxylic acid cycle was low in the first 9 days after birth (less than 4 per cent of the acid‐soluble 14C at 10 min after injection) and increased rapidly until 15 days when the level characteristic of the adult was approached (about 20 per cent of the acid‐soluble 14C). The results indicated that the oxidation of acetyl‐CoA derived from leucine reached the adult level at an earlier age than that derived from glucose.(3) The glutamine/glutamate specific radioactivity ratio was 0·3 in the brain of newborn animals and increased progressively; it was 1·3 and 2·4 at 15 and 35 days of age respectively. The specific radioactivity of aspartate and of GABA relative to that of glutamate was less than 1 throughout the experimental period.(4) The factors involved in the development of metabolic compartmentation in brain were analysed. It is proposed that although the experimental results show that a 'small’compartment becomes functionally manifested with maturation the primary cause is the development of the‘large’metabolic compartment.(5) Morphological correlates of the metabolic compartments in brain tissue are suggested and it is concluded that the manifestation of metabolic compartmentation is related to maturational changes in glia‐neuronal relations rather than to developmental processes affecting the individual components only.
COMPARTMENTATION OF CITRIC ACID CYCLE METABOLISM IN BRAIN: LABELLING OF GLUTAMATE, GLUTAMINE, ASPARTATE AND GABA BY SEVERAL RADIOACTIVE TRACER METABOLITES1
Authors: Berl S. , Nicklas W. J. , Clarke D. D. 
Published: October 2006

Abstract—(1) Compartmentation of the metabolism of amino acids in brain has been studied in slices of cerebral cortex incubated with sodium [1‐14C]acetate, sodium [1‐14C]‐bicarbonate, [1‐14C]GABA or l‐[1‐14C]glutamate and in samples of brain after injection in vivo of [1‐14C]‐ or [3H]acetate.(2) The method of treatment of the slices (a) maintained in ice‐cold medium prior to incubation; (b) preincubation at 37°C and transfer to fresh medium affected the metabolism of the added, labelled substrate, particularly its labelling of glutamine.(3) The specific activity of glutamine labelled from the above metabolites was greater than that of glutamic acid in experiments of 10–30 minutes duration, whether or not subjected to pretreatment in the cold.(4) Incubation in medium containing 27 mm‐K+ was associated with a decrease in the relative specific activity (RSA) of glutamine, except for the increase when l‐[1‐14C]glutamate was the precursor.(5) The data have been discussed in terms of metabolic compartmentation and their consistency with the concept of the presence in brain of more than one citric acid cycle, one containing the relatively smaller pools of intermediates and associated with synthetic processes; the other containing the relatively larger pools of intermediates and functioning as a homeostatic buffer for energy metabolism.
dl‐[2‐14C]p‐CHLOROPHENYLALANINE AS AN INHIBITOR OF TRYPTOPHAN 5‐HYDROXYLASE
Authors: Gál E. M. , Roggeveen A. E. , Millard S. A. 
Published: October 2006

Abstract—The distribution in vivo of dl‐[2‐14C]p‐chlorophenylalanine (p‐CP) in regions and subcellular fractions of the rat brain was determined. The half‐lives of p‐CP and its metabolite p‐chlorophenylpyruvic acid (p‐CPPA) in plasma and brain were correlated with the development of inhibition of cerebral tryptophan 5‐hydroxylase (EC 1.99.1.4). There was active transamination in vivo of p‐CP and p‐CPPA in the brain. Transport of indolealkylamino acids into brain was impaired by p‐CP. Inhibition of tryptophan 5‐hydroxylase could not be reversed by administration of large doses of l‐tryptophan, l‐tyrosine, or l‐phenylalanine. After administration of [2‐14C]p‐CP in vivo, appreciable radioactivity was bound to cerebral proteins, including those with tryptophan 5‐hydroxylase activity, as well as to phenylalanine 4‐hydroxylase (EC 1.99.1.2) purified from liver. Amino acid analysis of the acid hydrolysate of purified, radioactive hepatic phenylalanine 4‐hydroxylase showed over 80 per cent of the radioactivity to be present as p‐CP.Neither the inhibition in vivo nor in vitro of tryptophan 5‐hydroxylase could be reversed by dialysis; in controls, dialysis resulted in marked loss of enzyme activity. After incubation for 5 min with p‐CP in vitro, enzymic activity was inhibited 60 per cent. In vitro, p‐CPPA labelled protein much more extensively than p‐CP, yet inhibited the enzyme less. Some of the label from p‐CPPA was removable by dialysis.
THE DIFFERENTIATION OF PHOSPHOLIPASE A1 AND A2 IN RAT AND HUMAN NERVOUS TISSUES
Authors: Cooper Mary F. , Webster G. R. 
Published: October 2006

Abstract—Lipid‐free extracts of rat and human brain have been prepared and shown to contain phospholipase A1 and A2 activities and a lysophospholipase. The phospholipase Aj activity has pH optima of 4·2 and 4·6 in rat and human brain, respectively; it can be partially purified and isolated in high yields by dialysing the extracts at low pH. The purified preparations hydrolyse the ester bond at the 1‐position in lecithin, phosphatidyl‐ethanolamine and phosphatidylserine, but have little or no action on triglyceride or cholesterol ester. An assay system for the enzyme is described.Phospholipase A2 activity is optimal at pH 5·5 in rat brain extracts and at pH 5·0 in extracts of human brain. The phospholipase A2 activity of human cerebral cortex is largely unaffected by heating extracts at 70°C for 5 min, whereas this treatment substantially inactivates phospholipase A1 and completely destroys lysophospholipase.Phospholipase A1 is widely distributed in both grey and white matter of human brain and is also present in peripheral nerve. Phospholipase A2 activity is lower than A1 in all regions of the CNS examined so far, and is absent from peripheral nerve. Neither enzyme appears to require Ca2+ but both are inhibited by di‐isopropylfluorophosphate (DFP, 2 × 10−6 m) and thus differ from phospholipase A of pancreas.These studies confirm that the phospholipase A1 and A2 activities in brain are due to separate enzymes.
NORADRENALINE METABOLIZING ENZYMES IN NORMAL AND SYMPATHETICALLY DENERVATED VAS DEFERENS
Authors: Jarrott B. , Iversen L. L. 
Published: October 2006

Abstract—A surgical technique for sympathetically denervating the vas deferens has been evaluated biochemically. A slight fall in soluble muscle protein content and no significant change in DNA content of the operated vas deferens were found. This indicates that the surgical procedure causes only a slight degree of tissue damage and may be useful for investigating the cellular localization and properties of noradrenaline metabolizing enzymes. In three species examined (rat, guinea pig and rabbit), monoamine oxidase activity of the vas deferens fell by approximately 50 per cent after denervation. The time course of the fall in monoamine oxidase activity of rat vas deferens was parallel to that of the disappearance of noradrenaline suggesting that this proportion of the total enzyme activity had a neuronal localization. The remaining enzyme activity is presumably located extraneuronally.Significant falls in catechol‐O‐methyl transferase activity were found in rat and rabbit vas deferens after denervation but not in guinea pig. The rabbit and rat vas deferens had respectively approximately 60 and 30 per cent of the catechol‐O‐methyl transferase activity associated with the sympathetic nerves. A complete loss of DOPA decarboxylase and tyrosine hydroxylase activities occurred in rat vas deferens after denervation, suggesting that these noradrenaline synthesizing enzymes have an entirely neuronal localization.
THE EFFECT OF VOLATILE ANAESTHETICS ON LEVELS OF METABOLITES AND ON METABOLIC RATE IN BRAIN1
Authors: Brunner E. A. , Passonneau Janet V. , Molstad C. 
Published: October 2006

Abstract—Anaesthesia with ether, halothane, methoxyflurane (Penthrane) and Ohio 347 (Ethrane) increased the energy stores in mouse brain as much as 1·7‐fold above the control values. The greatest increases were observed in glucose and glycogen. Glucose‐6‐P was increased in some cases and UDP glucose was consistently lower in the anaesthetized animals. Hypothermia in conjunction with anaesthesia modified some of the observed changes. Hypothermia alone was associated with an increase in P‐creatine and glucose and a decrease in UDPglucose in the brain.The cerebral metabolic rate was depressed by all the anaesthetic agents to about 50 per cent of the control value. When the body temperature was lowered to 25°, the cerebral metabolic rate fell to 73 per cent of the control rate. A temperature coefficient of 1·035 was calculated as the fractional change/degree between 25° and 34°.
THE EFFECT OF ELECTROSHOCK ON REGIONAL CNS ENERGY RESERVES IN MICE1
Authors: Ferrendelli J. A. , McDougal D. B. 
Published: October 2006

AbstractATP, phosphocreatine, glycogen, glucose and lactate levels were measured in the cerebral cortex, thalamus, cerebellum, brain stem and spinal cord of mice following supramaximal electroshock. During the initial 17 s after the onset of a 2 s electrical stimulus high energy phosphate expenditure exceeded formation in all regions but was slower in spinal cord than in the other regions. In cerebral cortex high energy phosphate utilization continued to exceed formation for 32 s which was twice as long as in any other region studied. Altered levels of metabolites recovered most rapidly in spinal cord and least rapidly in cerebral cortex. Pretreatment with a non‐anaesthetic dose of phenobarbitone influenced the effect of electroshock. Most of the clinical seizure was prevented, and increased high energy phosphate utilization was sustained for a much shorter period. Only in cerebral cortex did high energy phosphate expenditure exceed formation for as long as 15 s after the electrical stimulus; but even in this region the excess of expenditure over formation was much less than in untreated animals.
BIOCHEMICAL STUDIES IN CAT AND HUMAN GANGLIOSIDOSIS1, 2
Authors: Handa S. , Yamakawa T. 
Published: October 2006

AbstractThe biochemical analysis of the hereditary neurological disease found in a family of Siamese cat is reported. The accumulation of GM1ganglioside in the brain was noted. Several glycosidase activities of these cat brains were compared with that of human gangliosidoses (Tay‐Sachs disease and GM1‐gangliosidosis). Glycosidase activities were estimated using ρ‐nitrophenyl‐glycosides, glucosyl‐, galactosyl‐ceramide and GM1‐ganglioside as substrates. The results indicated the defect of the β‐galactosidase activities for the ρ‐nitrophenyl‐β‐galactoside and GM1‐ganglioside in both cat and human GM1‐gangliosidoses. Glycosidase activities for glucosyl‐ and galactosyl‐ceramide were not changed in either gangliosidoses.
THE EFFECTS OF PYRIDOXINE DEFICIENCY AND OF CALORIC RESTRICTION ON LIPIDS IN THE DEVELOPING RAT BRAIN1
Authors: Williamson Barbara , Coniglio J. G 
Published: October 2006

Abstract— The effects of dietary deficiency of pyridoxine upon the contents of lipids in the brain were determined at several times after birth for three groups of rats. The mothers of the nursing pups were fed one of the following dietary regimes: pyridoxine‐deficient diet ad lib., pyridoxine‐supplemented diet ad lib., or pyridoxine‐supplemented diet in restricted amounts. At 7 and 14 days of postnatal age there were no significant differences between supplemented and deficient animals for any of the cerebral lipids studied. At 21 days the content of sphingomyelin in the brains of deficient animals was significantly lower than that in brains from the supplemented or calorically restricted animals in terms of percentage of total lipid and phospholipid phosphorus or tissue weight. On a per brain basis the content of sphingomyelin in the brains of calorically‐restricted rats was significantly lower than in the brains of rats fed the supplemented diet ad lib. The contents of cerebrosides but not of sulphatides or ceramides were also significantly lower in brains of the deficient group than in brains from the other two groups.The contents of pyridoxine in brains and in livers of the deficient animals were considerably lower than the contents found in the same organs of the other dietary groups. The results suggest that one reason for the abnormal development of the brains of rats on a pyridoxine‐deficient diet during the early postnatal period may be due to decreased quantities of sphingolipids.
N‐ACETYL‐l‐ASPARTIC ACID CONTENT OF HUMAN NEURAL TUMOURS AND BOVINE PERIPHERAL NERVOUS TISSUES
Authors: Nadler J. V. , Cooper J. R. 
Published: October 2006

Abstract— Abstract‐Tumors of the human nervous system were utilized to investigate the cellular distribution of N‐acetyl‐L‐aspartic acid (NAA). Astroglial tumours contained about 0.144 μmol/g. Oligodendrogliomas and medulloblastomas contained somewhat larger amounts. However, the level of NAA in all gliomas studied was less than that of normal human white matter. NAA was undetectable in meningiomas and acoustic neurinomas. If these results may be taken as representative of normal tissue, they imply a predominantly neuronal localization for NAA.Substantial amounts of NAA were found in peripheral nervous tissues and retina. Neurons seem to vary widely in NAA content.
ADENOSINE KINASE OF MAMMALIAN BRAIN: PARTIAL PURIFICATION AND ITS ROLE FOR THE UPTAKE OF ADENOSINE
Authors: Shimizu H. , Tanaka S. , Kodama T. 
Published: October 2006

Abstract— Adenosine metabolism in the homogenate of brain mainly undergoes deamination to inosine and hypoxanthine, while uniformly labelled [14C]adenosine injected into the carotid artery or [8‐14C]adenosine incubated with brain slices was mostly phosphorylated to [14C]adenine nucleotides in brain cells. Adenosine kinase has now been partially purified from homogenates of guinea pig brain. The kinase preparation was free of adenosine deaminase, almost free of adenosine triphosphatase and had a Km of the order of 2 × 10‐5M for adenosine.Kinetic studies with brain slices showed that adenosine reached the cells by diffusion and that the diffusion was facilitated by subsequent phosphorylation to adenine nucleotides. From the following experimental results, it is concluded that the phosphorylation is catalysed by adenosine kinase quantitatively. (1) During the uptake and phosphorylation of adenosine by brain slices, the nucleoside did not split to adenine and ribose moieties. (2) The rate of formation of adenine nucleotides in the slices was a hyperbolic function of the concentration of adenosine in the medium, showing an apparent Km foradenosine of the order of 2 × 10‐5 M. (3) Some analogues of adenosine inhibited both the facilitated diffusion of adenosine and the kinase activity, but ouabain (0.005 mM) did not inhibit either.
HISTAMINE FORMATION IN RAT BRAIN IN VIVO: EFFECTS OF HISTIDINE LOADS12
Authors: Schwartz J. C. , Lampart C. , Rose C. 
Published: October 2006

Abstract— Administration of l‐histidine at the rate of 500 mg/kg induced an increase of nearly 50 per cent in the level of histamine in rat brain which lasted several hours. The augmentation of histamine level was not significant 3 h after lower doses or after d‐histidine α‐methyl DOPA and Ro 4‐4602 neither affected the cerebral level of histamine nor its elevation induced by l‐histidine. Brocresine, a known histidine decarboxylase inhibitor not only prevented the effect of histidine load but also induced a prompt fall in the amine level. These results confirm those from earlier experiments in vitro indicating that histamine synthesis in rat brain depends on a specific decarboxylase (EC 4, 1.1.22) which is not normally saturated by the endogenous level of its substrate.When histamine levels were enhanced by histidine treatment, histidine decarboxylase activity, as evaluated on hypothalamus homogenates, was significantly reduced; intracisternal administration of cycloheximide, an inhibitor of protein synthesis, had similar effects. On the other hand, enzyme activity was not altered by the addition of histamine to hypothalamus homogenates. These results are compatible with the existence of a regulation mechanism of histidine decarboxylase involving repression by its end‐product.
UPTAKE OF [3H‐METHYL]CHOLINE BY MICROSOMAL, SYNAPTOSOMAL, MITOCHONDRIAL AND SYNAPTIC VESICLE FRACTIONS OF RAT BRAIN
Authors: Diamond I. , Milfay D. 
Published: October 2006

Abstract— Microsomal, mitochondrial, synaptosomal and synaptic vesicle fractions of rat brain took up [3H‐methyl]choline by a similar carrier‐mediated transport system. The apparent Km for the uptake of [3H‐methyl]choline in these subcellular fractions was about 5 × 10−5 M. Choline uptake was also observed in microsomal fractions prepared from liver and skeletal muscle. Virtually identical kinetic properties for [3H‐methyl]choline transport were found in the synaptosomal fractions prepared from the whole brain, cerebellum or basal ganglia. Countertransport of [3H‐methyl]choline from the synaptosomal fraction was demonstrated against a concentration gradient. HC‐3 was a competitive inhibitor of the uptake of [3H‐methyl]choline in brain microsomal, synaptosomal and mitochondria] fractions with respective values for Ki of 4.0, 2.1 and 2.3 × 10−5 M. HC‐15 was a competitive inhibitor of the transport of [3H‐methyl]choline in the synaptosomal fraction, with a Ki of 1.7 × 10−4 M. Upon entry into the microsomal fraction, 74 per cent of the radioactivity could be recovered as unaltered choline, 10 per cent as phosphorylcholine, 1.5 per cent as acetylcholine and 2.5 per cent as phospholipid.Choline acetyltransferase (EC 2.3.1.6) was assayed with [14C]acetylCoA in synaptosomal fractions prepared from basal ganglia and cerebellum, and in the 31,000 g supernatant fraction of a rat brain homogenate. Enzyme activity was 11‐fold greater in the synaptosomal fraction from the basal ganglia than in that from the cerebellum. HC‐3 did not inhibit choline acetyltransferase and there was no evidence for acetylation of HC‐3.Our findings suggest that choline uptake is a ubiquitous property of membranes in the CNS and cannot serve to distinguish cholinergic nerve endings and their synaptic vesicles.
TRYPTOPHAN 5‐HYDROXYLASE: APPROXIMATION OF HALF‐LIFE AND RATE OF AXONAL TRANSPORT
Authors: Meek J. L. , Neff N. H. 
Published: October 2006

Abstract—The half‐life of tryptophan 5‐hydroxylase (EC 1.14.3) in rats was estimated from the return of enzyme activity after administration of p‐chlorophenylalanine and from the decline of enzyme activity in spinal cord after transection or an intraspinal injection of colchicine. The half‐life was 2–3 days. Axonal transport of enzyme, estimated from the reappearance of activity in consecutive portions of spinal cord after treatment with p‐chlorophenylalanine, was of the order of 5–7 mm/day. This rate is characteristic of 'slow’axonal flow. Our results suggest that changes in the synthesis of new enzyme are probably not responsible for acute changes in the turnover of serotonin.