bluuebunny/crossref_metadata_2025_split huggingface dataset:
DHPOSITION OF LIPIDS IN THE DEVELOPING CENTRAL AND PERIPHERAL NERVOUS SYSTEMS OF THE CHICKEN
Authors: Shaikh Nisar A. , Palmer F. B. St. C. 
Published: October 2006

Abstract— The lipid composition of chick brain and sciatic nerve was determined during development. It was confirmed that the addition of CaCl2 to solvents during the extraction of lipids from brain results in much higher yields of diphosphoinositides particularly from unmyelinated embryo brain. Unlike the earlier report for rat brain, the recovery of triphosphoinositides was also Substantially increased. The amount of CaCl2, required to achieve optimal recoveries decreased with increasing age and addition of more than this optimal amount depressed the yields of polyphosphoinositides, particularly triphosphoinositides. CaCl2, addition did not improve the yield of diphosphoinositides from sciatic nerve of any age but drastically reduced recovery of triphosphoinositidcs. Differenccs in the effect of CaCl2 were not the result of variation in the tissue concentrations of calcium or magnesium.The lipid composition of sciatic nerve closely reflected that of the myelin. Both polyphosphoinositides were absent initially and their accumulation paralleled that of cerebrosides and sulfatides. The concentration of diphosphoinositides remained constant after the period of most active myelination while triphosphoinositides and the galactolipids continued to increase suggesting maturational changes in the myelin composition. The pattern of deposition in chick brain was similar except for the much greater contribution of non‐myelin structures. Both polyphosphoinositides were present in equimolar amounts in pre‐myelination embryonic tissue. The concentration of diphosphoinositides increased during active myelination only while triphosphoinositides continued to increase thereafter.
TRANSCRIPTION OF REPEATED AND UNIQUE DNA SEQUENCES IN BRAIN NUCLEI
Authors: Soga K. , Takahashi Y. 
Published: October 2006

Abstract—Transcription of repeated and unique DNA in rat brain nuclei was examined using a RNA‐DNA hybridization technique. Saturation hybridization experiments with a membrane filter showed that there were differences in the base sequence complements between labelled brain and labelled liver nuclear RNA. In competition hybridization experiments using a membrane filter, brain nuclear labelled RNA was in competition most effectively with unlabelled brain nuclear RNA, but less effectively with kidney or liver nuclear RNA. Experiments using a membrane filter loaded with isolated unique or repeated DNA fragments gave similar results. Furthermore, competition hybridization with a DNA excess also showed similar results at Cot 10,000. These results indicate the existence of tissue‐specificity in the transcription of unique and repeated DNA sequences in brain nuclei. Subsequently, rat brain nuclei were separated into neuronal and glial nuclear fractions for the purpose of detecting the cell‐specificity of RNA. The results of these experiments give evidence of significant differences in the transcription of unique DNA sequences, but indicate no differences in that of repeated DNA sequences between the two nuclear classes.
UPTAKE OF NEUROTRANSMITTER CANDIDATES BY PIGEON OPTIC TECTUM
Authors: Henke H. , Schenker T. M. , Cuenod M. 
Published: October 2006

Abstract—The kinetics of the uptake of various compounds into the crude mitochondrial fraction (P2‐fraction) of the pigeon optic tectum were studied. Aspartate, GABA, glutamate, glycine, proline and choline were taken up by high and low affinity systems. Only low affinity uptake was found for leucine and dopamine. The uptake for taurine was not saturable. The uptakes for all of the above compounds were temperature and sodium dependent. The high affinity system was more effected by sodium withdrawal than the low affinity system. Continuous sucrose gradients from 0.4 to 1.5 m were run with incubated P2 fractions. Particle‐bound radioactivity sedimented in a density range of 1.0 to 1.2 m‐sucrose. Additional experiments with glutamate showed that its uptake is competitively inhibited by aspartate. The addition of a 1000‐fold excess of glutamate to a P2 fraction incubated at a concentration of 10–6m‐glutamate led to a massive decrease of particle‐bound radioactivity, suggesting a coupled action of uptake and efflux.
EFFECTS OF RETINAL ABLATION ON UPTAKE OF GLUTAMATE, GLYCINE, GABA, PROLINE AND CHOLINE IN PIGEON TECTUM
Authors: Henke H. , Schenker T. M. , Cuenod M. 
Published: October 2006

Abstract—The effect of retinal ablation on the high and low affinity uptake of choline, GABA, glutamate, glycine and proline into the crude mitochondrial fraction of the pigeon optic tectum was studied. After 4–8 weeks of degeneration the uptake for glutamate, and to a lesser degree the uptake for GABA, at both the high and the low affinity substrate concentration, decreased. In contrast, the uptake of glycine increased. Kinetic analysis showed that the reduced uptake of glutamate was due to a decrease in the Vmax. By intraocular injection of [3H]proline the retinal endings in the optic tectum were labelled with the fast axoplasmic transport fraction. Optic terminals labelled in this way have the same sedimentation characteristics in continous sucrose gradients as the particles accumulating giutamate in the uptake assay.
ROLE OF RIBONUCLEASE ACTION IN PHENYLALANINE‐INDUCED DISAGGREGATION OF RAT CEREBRAL POLYRIBOSOMES
Authors: Roberts S. , Morelos Beatrice S. 
Published: October 2006

Abstract—l‐phenylalanine (1 mg/g body wt) or physiological saline (0.9% NaCl) was given intraperitoneally to infant (7‐day old), immature (14‐day old), and adult (42‐day old) rats. The state of ribosomal aggregation was determined in the cerebral postmitochondrial supernatant and purified polyribosome fractions prepared in the presence of rat liver ribonuclease inhibitor. Polyribosomes isolated from cerebral cortices of infant and immature rats 30 or 60 min after administration of phenylalanine were partially disaggregated, whereas the state of aggregation of polyribosomes from mature cerebrum was unchanged. In contrast, little or no evidence of phenylalanine‐induced polyribosome disruption was noted in the postmitochondrial supernatant fractions, from which the cerebral polyribosomes were prepared, in any of the animals. Omission of the ribonuclease inhibitor resulted in polyribosome disaggregation in the postmitochondrial supernatant fractions prepared from saline‐treated as well as phenylalanine‐treated infant rats, but the disruption was more profound in the latter group. Ribonuclease activities in cerebral postmitochondrial supernatant preparations from infant and immature rats were higher than the corresponding values in preparations from adult animals. In addition, the administration of phenylalanine resulted in increases in ribonuclease activities in cerebral postmitochondrial supernatant preparations from the younger animals, but had no effect on these activities in adult animals. These results suggest that alterations in structure and function of polyribosomes from the infant rat cerebrum following a loading dose of phenylalanine were related to exposure of the polyribosomes during isolation to elevated activities of cerebral ribonucleases resulting from this treatment. This hypothesis was supported by the finding that phenylalanine treatment had no effect on the incorporation in vivo of intracisternally‐administered radioactive lysine into total, soluble or ribosomal protein of infant cerebrum. However, when cerebral ribosomal RNA was differentially labelled in phenylalanine‐treated and saline‐treated infant rats by the intracisternal administration of [3H] or [14C]uridine, and polyribosome fractions were then prepared from the pooled cerebral cortices of both groups, radioactive ribosomes derived from saline‐treated rats were more highly aggregated than those derived from phenylalanine‐treated animals. It is concluded that gross alterations in cerebral polyribosome structure and function do not occur in vivo in young rats given a large amount of phenylalanine intraperitoneally. However, this treatment, in addition to increasing ribonuclease activity in cerebral cell‐free preparations, also sensitizes cerebral polyribosomes to subsequent breakdown upon exposure to ribonucleases during isolation.
THE RELEASE OF BRAIN FREE FATTY ACIDS DURING ISCHAEMIA IN ESSENTIAL FATTY ACID‐DEFICIENT RATS
Authors: Galli C. , Spagnuolo C. 
Published: October 2006

Abstract—The release of free fatty acids and especially of free arachidonic acid occurring in rat brain during ischaemia has been studied in essential fatty acid‐deficient animals. Free fatty acid levels are lower in essential fatty acid‐deficient brains before and especially after 5 min of ischaemia. The percentage of arachidonic acid, in respect of total free fatty acids, is similar in both control and essential fatty acid‐deficient brains before ischaemia (0 min), but is greatly reduced in deficient brains in respect of controls after ischaemia (5 min). Total levels of free arachidonic acid are thus greatly reduced after ischaemia in the brain of essential fatty acid‐deficient rats. Focussed microwave irradiation of the brain, a technique which instantaneously kills the animals, and which was used for the determination of brain basal levels of free fatty acids and free arachidonic acid, does not per se modify brain lipid and fatty acid composition.
THE EFFECT OF HYPERTHERMIA UPON OXYGEN CONSUMPTION AND UPON ORGANIC PHOSPHATES, GLYCOLYTIC METABOLITES, CITRIC ACID CYCLE INTERMEDIATES AND ASSOCIATED AMINO ACIDS IN RAT CEREBRAL CORTEX
Authors: Carlsson C. , Hägerdal M. , Siesjö B. K. 
Published: October 2006

Abstract—The influence of hyperthermia on cerebral blood flow, cerebral metabolic rate for oxygen and cerebral metabolite levels was studied by increasing body temperature from 37° to 40°C and 42°C in rats under nitrous oxide anaesthesia maintained at constant arterial CO2 tension. The metabolic rate for oxygen increased by 5‐6% per degree centigrade. At 42°C the increase in cerebral blood Row was comparable to that in the metabolic rate. The increased temperatures were not accompanied by changes in organic phosphates (phosphocreatine, ATP, ADP or AMP) or in lactate/pyruvate ratio. There was an increase in the tissue to blood glucose concentration ratio. At steady state, there was an increase in glucose‐6‐phosphate but no other changes in glycolytic metabolites or citric acid cycle intermediates, and the only change in amino acids studied (glutamate, glutamine, aspartate, alanine and GABA) was an increase in glutamate concentration.
STABILITY OF ENZYMES IN POST‐MORTEM RAT BRAIN1
Authors: Fahn S. , Côté L. J. 
Published: October 2006

Abstract—Enzyme activities were measured in rat brains kept at room temperature for various intervals after death by decapitation. Tytosine hydroxylase, monoamine oxidase, choline acetyltransferase, and acetylcholinesterase show a substantial decline in activity over 14h reaching 64, 78, 60 and 58%, respectively. of the zero‐time activity. DOPA decarboxylase, glutamic acid decarboxylase, lactate dehydrogenase, Na‐K‐ATPase and Mg‐ATPase show less than a 15% decline in activity. The activities of most of the enzymes studied show little change time period when human brain specimens are likely between the 6th and 14th hour after death, the to be obtained for biochemical studies
POST‐ISCHEMIC CHANGES IN CERTAIN METABOLITES FOLLOWING PROLONGED ISCHEMIA IN THE GERBIL CEREBRAL CORTEX
Authors: Mrsulja B. B. , Lust W. D. , Mrsulja B. J. , Passonneau J. V. , Klatzo I. 
Published: October 2006

Abstract‐Eight metabolites were measured in the post‐ischemic period following either 1 or 3 h of unilateral ischemia in the gerbil cerebral cortex. The levels of ATP, P‐creatine, glucose, glycogen and GABA were essentially restored by 1 h after ischemia. In the 3 h ischemic animals. glycogen continued to increase to greater than control values aftcr 5 and 20 h of recirculation. The Icvels of glutamate were unchanged during the ischemic episode, but decreased to 60% of control at Smin and 1 h after either period of ischemia. The concentrations of cyclic AMP, which were 4‐to 5‐fold elevated during ischemia. increased an additional 6‐fold 5 min after recirculation in both groups. Arter 1 h of recovery. the levels were not different from control values. After the 1 h ischemic period, lactate levels recovered between 5 and 20 h of recirculation. In the 3 h ischemic animals. lactate concentrations were still elevated even after 20 h of recirculation. These data suggest that with the exception of lactate. recovery of metabolites is not sevcrely compromiscd by either 1 or 3 h of ischemia. Furthermore, the changes in glycogen. glutamate and cyclic AMP after recirculation suggest that the recovery process is not just a rcversal of the changes observed during ischemia.
THE EFFECTS OF PHENYLALANINE ON AMINO ACID METABOLISM AND PROTEIN SYNTHESIS IN BRAIN CELLS IN VITRO1
Authors: Hughes J. V. , Johnson T. C. 
Published: October 2006

AbstractIncubation of brain cell suspensions with 14 mM‐phenylalanine resulted in rapid alterations of amino acid metabolism and protein synthesis. Both thc rate of uptake and the final intracellular concentration of several radioactively‐labelled amino acids were decreased by high concentrations oi phenylalanine. By prelabelling cells with radioactive amino acids, phenylalanine was also shown to effect a rapid loss of the labelled amino acids from brain cells. Amino acid analysis after the incubation of the cells with phenylalanine indicated that several amino acids were decreased in their intracellular concentrations with effects similar to those measured with radioisotopic experiments (large neutral > small and large basic > small neutral > acidic amino acids). Although amino acid uptake and efflux were altered by the presence of 14 mwphenylalanine, little or no alteration was detected in the resulting specific activity of the intracellular amino acids. High levels of phenylalanine did not significantly altcr cellular catabolism of either alanine, lysine, leucine or isoleucine. As determined by the isolation of labcllcd aminoacyl‐tRNA from cells incubated with and without phenylalanine, there was little or no alteration in the level of this precursor for radioactive alanine and lysine. There was, however, a detectable decrease in thc labelling of aminoacyl‐tRNA for leucine and isoleucine. Only aftcr correcting for the changes of the specific activity of the precursors and thcir availability to translational events, could the effects of phenylalanine on protein synthesis be established. An inhibition of the incorporation into protein for each amino acid was approximately 20%.
SELECTIVE LOCALIZATION OF A HIGH AFFINITY CHOLINE UPTAKE SYSTEM AND ITS ROLE IN ACh FORMATTON IN CHOLINERGIC NERVE TERMINALS
Authors: Suszkiw J. B. , Pilar G. 
Published: October 2006

AbstractThe avian iris‐ciliary nerve preparation exhibits two distinct choline uptake systems. One component, a sodium dependent, high affinity system Km‐2 am and Vmax ‐ 0.5 pmolpin per preparation is confined to nerve terminals. The other component is localized in muscle cells. It is sodium independent and low affinity system (Km ‐ 200 am and Vmax ‐ 16 pmol/min per muscle). The high affinity uptake of choline and the synthesis of ACh in the nerve terminals are coupled. Vmax Ach formation ‐0.5 pmol/min. is the same as Vmax for choline transport; however. with the external choline concentration equal to that of avian plasma only ‐50% of choline taken up is converted to ACh. In contrast to the nerve terminals, the cell bodies of the same neurons are deficient in the high affinity uptake‐ACh synthesis coupled system. This indicates a nerve terminal membrane specialization related to neuro‐transmitter synthesis.
PURIFICATION OF NERVE GROWTH FACTOR ANTIBODIES BY AFFINITY CHROMATOGRAPHY
Authors: Stoeckel K. , Gagnon C. , Guroff G. , Thoenen H. 
Published: October 2006

AbstractPure antibodies to nerve growth factor have been isolated from sheep nerve growth factorantiserum by affinity chromatography using 2.5 S nerve growth factor linked to Sepharose 4B by means of cyanogen bromide. The elution of the antibodies was accomplished either at low pH (pH 2) or by high salt concentration (4.5 wMgC12). The purity of the antibodies was established by SDS‐gel electrophoresis. Their immunological activity was tested by imrnunoprecipitation and their biological activity in a tissue culture assay using embryonic chick dorsal root ganglia.
DEVELOPMENT AND REGULATION OF LIPID SYNTHESIS FROM KETONE BODIES BY RAT BRAIN
Authors: Patel M. S. , Owen O. E. 
Published: October 2006

Abstract—Cerebral cortex slices from 1‐day old rats incorporated actively 3‐hydroxy[3‐14C] butyrate into lipids. The rate of synthesis increased moderately during the first postnatal week and then decreased rapidly reaching negligible rates by the end of the fourth postnatal week. The incorporation of [3‐14C]acetoacetate (5 mM) and 3‐hydroxy[3‐14C]butyrate (5 mM) at non‐physiological concentrations into lipids by cerebral cortex from 1‐week old rats was markedly stimulated in the presence of added glucose; however, the addition of glucose had no effect on the oxidation of ketone bodies to 14CO2 At physiological concentrations of acetoacetate (0.5 mM) and 3‐hydroxybutyrate (1 mM), glucose stimulated both the oxidation of ketone bodies to 14CO2 and the incorporation of ketone body‐carbon into cerebral lipids. In contrast, the oxidation of [U‐14C]glucose to CO2 and its incorporation into lipids by brain slices were markedly reduced in the presence of ketone bodies at physiological as well as non‐physiological concentrations. However, the total rate of lipid synthesis, as determined by the incorporation of 3H from 3H2O, was maintained under these conditions. This indicated that the decreased contribution of the acetyl moiety from glucose was compensated to a similar extent by acetyl‐CoA formed from ketone bodies. The findings show that both acetoacetate and 3‐hydroxybutyrate are better precursors than glucose for in vitros lipid synthesis in developing rat brain.
THE DISTRIBUTION OF GLYCINE, GABA, GLUTAMATE AND ASPARTATE IN RABBIT SPINAL CORD, CEREBELLUM AND HIPPOCAMPUS
Authors: Berger Sosamma J. , Carter Joyce G. , Lowry O. H. 
Published: October 2006

Abstract—The distribution of glycine, GABA, glutamate and aspartate was measured among about 60 subdivisions of rabbit spinal cord, and among the discrete layers of cerebellum, hippocampus and area dentata. A more detailed mapping for GABA was made within the tip of the dorsal horn of the spinal cord. Spinal ventral horn and dorsal root ganglion cell bodies were analyzed for the amino acids and for total lipid. The distribution of lipid and lipid‐free dry weight per unit volume was also determined in spinal cord. Calculated on the basis of tissue water, glycine in the cord is highest in lateral and ventral white matter immediately adjacent to the ventral grey. The distribution of GABA is almost the inverse of that of glycine with highest level in the tip of dorsal horn. It is most highly concentrated in the central 75% of Rexed layers III and IV. Aspartate in the tip of ventral horn is 4‐fold higher than in the tip of the dorsal horn and 3 times the average concentration in brain. Glutamate was much more evenly distributed and is relatively low in concentration with slightly higher levels in dorsal than in ventral grey matter. Large cell bodies in both ventral horn and dorsal root ganglion contained high levels of glycine. As reported by others, GABA was found to be high in cerebellar grey layers, area dentata, and regio inferior of hippocampus. Glycine was moderately high in cerebellar layers but moderate to low in hippocampus and area dentata.
ARGINASES OF MOUSE BRAIN AND LIVER
Authors: STEWART J. A. , CARON H. 
Published: October 2006

AbstractThe arginase present in mouse brain and liver was studied in order to determine if the activity in both tissues was due to the same enzyme. Mouse liver contains only one arginase enzyme whereas mouse brain contains two. One of the arginases in the brain is distinct from the liver enzyme as determined by fractionation on DEAE‐cellulose, CM‐cellulose and disc gel electrophoresis. The second enzyme from brain tissue has the same properties as the liver enzyme when subjected to these same fractionation techniques. However this arginase can be distinguished from the liver enzyme by its Km for arginine heat lability and MnCl2 activation curve. Thus both arginases in brain differ from the liver enzyme.No interconversion of the brain enzymes was detected, and the molecular weight of all the arginases appears to be the same. The observation of multiple distinct brain and liver arginases in mouse brain and liver was confirmed with bovine tissues.
ALTERATIONS IN RECEPTORS CONTROLLING DOPAMINE SYNTHESIS AFTER CHRONIC ETHANOL INGESTION
Authors: Tabakoff Boris , Hoffman Paula L. 
Published: October 2006

AbstractThe influence of acute and chronic ethanol treatment and withdrawal on regulation of dopamine synthesis in striatal and mesolimbic areas of mouse brain was evaluated. Tyrosine hydroxylase activity was estimated by measuring in vivo DOPA accumulation after inhibition of aromatic amino acid decarboxylase. Eight hours after a single (3 g/kg) dose of ethanol, DOPA synthesis was increased and pimozide, a dopamine receptor antagonist, stimulated DOPA synthesis to the same degree in ethanol‐treated and control animals. On the other hand, 8 h after withdrawal of animals from chronic ethanol treatment, endogenous dopamine synthesis was the same in ethanol‐withdrawn and control animals, but the stimulation of dopamine synthesis produced by low doses of pimozide or haloperidol was significantly less in the animals that had consumed ethanol. This effect was even more apparent at 24h after withdrawal; by 3 days after withdrawal the decreased response of ethanol‐withdrawn animals to the administration of dopamine receptor blockers was no longer statistically significant. At all time points tested, high doses of pimozide or haloperidol stimulated DOPA synthesis equally in control and ethanol‐withdrawn animals. Chronic ethanol treatment and withdrawal may alter the coupling between dopamine receptors which regulate dopamine synthesis and tyrosine hydroxylase.
ALTERATIONS IN GABA METABOLISM AND MET‐ENKEPHALIN CONTENT IN RAT BRAIN FOLLOWING REPEATED ELECTROCONVULSIVE SHOCKS
Authors: Green A. R. , Peralta E. , Hong J. S. , Mao C. C. , Atterwall C. K. , Costa E. 
Published: October 2006

AbstractThe effects of electroconvulsive shock (ECS; 120 V for 1 s through ear‐clip electrodes) or sub‐convulsive shocks (70 V for 1 s) on rat brain GABA and met‐enkephalin concentration and GABA turnover has been examined 24 h after a single treatment (×1) or once daily for 10 days (×10). ECS × 10 increased GABA concentrations in the N. caudatus and N. accumbens and decreased the synthesis rate of GABA by 40% and 50% respectively in these regions. Sub‐convulsive shocks (× 10 × 10) or ECS × 1 had no effect. No consistent changes were seen in the substantia nigra. Met‐enkephalin concentrations increased by 50% in the N. caudatus after ECS × 10 but were unchanged in the cortex and pons/medulla. No other shock regimen had any effect on the concentration of this peptide. The results are discussed in relation to the enhanced monoamine‐induced responses seen only after ECS × 10.