bluuebunny/crossref_metadata_2025_split huggingface dataset:
TRANSFER RNA AND THE REGULATION OF PROTEIN SYNTHESIS IN RAT CEREBRAL CORTEX DURING NEURAL DEVELOPMENT
Authors: Harris C. L. , Maas J. W. 
Published: October 2006

AbstractProtein synthesis was measured in ribosomal systems derived from the cerebral cortex of 5‐and 35‐day‐old rats. Under optimal conditions incorporation of radioactive leucine per mg ribosomal protein was four times higher with ribosomes from the younger animals than with ribosomes from the 35‐day‐old rats. This suggests that a decrease in the rate of protein synthesis occurs during neural development. Both ribosomes and the pH enzyme fraction from the cerebral cortex of 35‐day‐old rats had lower activities than preparations from the younger rats. Cerebral cortical ribosomes from 35‐day‐old animals had a lower polyribosome content than similar preparations from 5‐day‐old rats. A three‐fold higher requirement for the pH 5 enzyme fraction was observed with the ribosomal system from 5‐day‐old rats, an observation which correlated with the yields of pH 5 enzyme and ribosomal protein from the younger tissue.The nature of the changes in the composition of the pH 5 enzyme fraction was investigated. Methylated albumin kiesselguhr (MAK) and Sephadex G‐75 column chromatography showed that RNA from the pH 5 enzyme fraction was heterogeneous, containing tRNA, rRNA, and a small molecular weight RNA. This latter RNA, perhaps a degradation product of rRNA, comprised the greatest portion of RNA from the pH 5 enzyme fraction of cerebral cortex. The data obtained with MAK chromatography were used to estimate the total tRNA content of the cerebral cortex, with no age‐related differences being observed. Since evidence of RNA degradation was seen, tRNA was also isolated by phenol extraction of whole cerebral cortex in the presence of bentonite. Purification of tRNA by NaCl and isopropanol fractionation gave preparations with no detectable rRNA or small molecular weight RNA. With this purification method, the tRNA yield was greater than estimated by the MAK method, demonstrating that losses of tRNA occurred during the cell fractionation steps. With the purification method 1.6 times more tRNA was obtained from the cerebral cortex of 5‐day‐old animals than from the older tissue. This higher level of tRNA in the younger, more active tissue appeared to involve all tRNA species, since in vitro aminoacyiation studies revealed nearly identical acceptance values for 18 individual amino acids. These results suggest that the rate of protein synthesis in cerebral cortex is regulated in part by the total amount of tRNA present to translate the higher level of polysome‐bound mRNA.
β‐NEUROTOXIN REDUCES NEUROTRANSMITTER STORAGE IN BRAIN SYNAPSES
Authors: Wernicke J. F. , Oberjat T. , Howard B. D. 
Published: October 2006

Abstractβ‐neurotoxin, a component of Bungarus multicinctus venom, is known to cause neuromuscular blockade by first increasing the rate of spontaneous ACh release and then inhibiting the nerve impulse‐induced release of ACh. We report that the toxin also affects the storage of several neurotransmitters in rat brain and it is active on synaptosomes and brain minces. Synaptosomes prepared from brain tissue that had been treated with β‐toxin have a reduced ability to accumulate radioactive NE, GABA, serotonin and the ACh precursor, choline. The toxin also causes a release of previously accumulated NE and GABA from synaptosomes, suggesting that the storage process rather than the uptake transport process is affected. The toxin does not contain phospholipase A, phospholipase C, protease or hyaluronidase activity.
PATTERNS OF CHANGES IN BRAIN CARBOHYDRATE METABOLITES, AMINO ACIDS AND ORGANIC PHOSPHATES AT INCREASED CARBON DIOXIDE TENSIONS
Authors: Folbergrovaa Jaroslava , Pontean U. , Siesjou B. K. 
Published: October 2006

Abstract—In order to study the time course of changes in cerebral metabolites in hypercapnia, anaesthetized and artificially ventilated rats were exposed to 11% CO2 for 5, 15, 45, 90 and 180 min. In addition, the effect of anaesthetic levels of carbon dioxide was studied by exposing animals to 30 and 50% CO2 for 45 min. In none of the groups were there significant changes in ATP, ADP or AMP, and a normal energy state was therefore obtained even in short‐lasting hypercapnia, and at anaesthetic CO2 concentrations (50% CO2). In the group exposed to 11% CO2 for 5 min there was a fall in glycogen but normalization occurred when the hypercapnia was prolonged. There were no changes in fructose 1,6‐diphosphate, dihydroxyacetone phosphate or 3‐phosphoglycerate but decreases in pyruvate, lactate, citrate, α‐oxoglutarate, malate and glutamate at all exposure times. With 30 and 50% CO2 glucose 6‐phosphate accumulated. The results do not support the view that the depletion of pyruvate and of citric acid cycle intermediates is caused by H+‐inhibition of rate‐limiting enzymatic steps like the phosphofructokinase reaction.The glutamate concentration fell progressively during exposure to 11% CO2. In the 5 and 15 min groups aspartate increased significantly indicating that the initial loss of glutamate was partly due to transamination to aspartate. With prolonged hypercapnia there was a secondary fall in aspartate to subnormal values. At 45 min and thereafter the glutamine concentration increased significantly. However, the sum of glutamate, aspartate and glutamine fell progressively after the initial 5 min period.Hypercapnia gave rise to similar increases in the lactate/pyruvate and malate/oxaloacetate ratios, and since the calculated NADH/NAD+ ratios remained close to normal in all groups, the results indicate that pH‐dependent shifts occurred in the lactate and malate dehydrogenase equilibria.
PURINE NUCLEOTIDE METABOLISM IN THE CAT BRAIN AFTER ONE HOUR OF COMPLETE ISCHEMIA
Authors: Kleihues P. , Kobayashi K. , Hossmann K.‐A. 
Published: October 2006

Abstract—Complete cerebral ischemia was produced in normothermic anaesthetized cats by clamping the innominate and the left subclavian arteries combined with lowering the blood pressure. After 1 h of ischemia, ATP was no longer present in detectable amounts. Total adenine nucleotides were reduced to 34 per cent of the normal level. The breakdown of guanine nucleotides was less marked, with small amounts of GTP still being present at the end of the ischemic period. In animals with signs of functional recovery after 3–7 h of recirculation, ATP was resynthesized to 62 per cent of the control level. Total adenine nucleotides increased to 68 per cent and the adenylate energy change—[ATP + 1/2 ADP]/[AMP + ADP + ATP]—was re‐established to within 7 per cent of the pre‐ischemic value. Radiochromatography of nucleotides following intravenous injection of [14C]formate indicated a marked enhancement of postischemic purine de novo synthesis. Purine nucleosides and free bases which accumulated during ischemia, were partially re‐utilized by salvage pathways: adenosine was rephosphorylated to AMP by adenosine kinase (EC 2.7.1.20); inosine and hypoxanthine were re‐used via IMP in a reaction mediated by hypoxanthine phosphoribosyltransferase (EC 2.4.2.8).
CEREBRAL ENERGY STATE IN INSULIN‐INDUCED HYPOGLYCEMIA, RELATED TO BLOOD GLUCOSE AND TO EEG
Authors: Lewis L. D. , Ljunggren B. , Ratcheson R. A. , Siesjö B. K. 
Published: October 2006

Abstract—Concentrations of phosphocreatine, creatine, ATP, ADP and AMP were measured in the cerebral cortex of rats during insulin‐induced hypoglycemia. Blood glucose concentrations were related to clinical symptoms in unanaesthetized animals and to the EEG pattern in paralysed and lightly anaesthetized animals. There was an excellent correlation between blood glucose concentration and EEG pattern. In animals showing a pronounced slowing of the EEG or convulsive polyspike activity for up to 20 min, there were no changes in any of the phosphates. However, after prolonged convulsive activity some animals showed clear signs of energy failure, and in all animals with an isoelectric EEG there was a major derangement of the energy state. Since the majority of those animals did not show signs of cerebral hypoxia or ischemia it is concluded that hypoglycemic coma is accompanied by substrate deficiency of a degree sufficient to induce energy depletion of brain tissue.
RELEASE OF [3H]GAMMA‐AMINOBUTYRIC ACID FROM GLIAL CELLS IN RAT DORSAL ROOT GANGLIA.
Authors: Minchin M. C. W. , Iversen L. L. 
Published: October 2006

Abstract— Desheathed rat dorsal root ganglia were incubated in a medium containing amino‐oxyacetic acid and [3H]GABA. Under these conditions, [3H]GABA is taken up exclusively by the satellite glial cells in the ganglia. Efflux of [3H]GABA from the tissue was measured after passing the ganglia through a series of wash solutions. The spontaneous efflux of radioactivity, mostly [3H]GABA, was more rapid in the absence of amino‐oxyacetic acid in the incubation and wash media.Raising the potassium concentration in the wash media caused an increase in the efflux of [3H]GABA. This increase was sigmoidally related to the potassium concentration in the wash media, reaching a maximum at 64 mm‐K+. The releasing effect of K+ was inhibited by removing calcium from the media. Reducing the calcium and raising the magnesium concentration in the wash solutions inhibited the increased efflux of [3H]GABA due to 64 mm‐K+ by 48 per cent, while 5 mM‐La3+ and diphenylhydantoin (0·005 and 0·5 mm) had no effect on this increase.Only a small increase in the efflux of [14C]glutamate was produced by 64 mm‐K+ and it had no effect upon the effluxes of [3H]glycine, [3H]alanine or [3H]leucine. The efflux of lactate dehydrogenase was similarly unaffected by 64 mM‐K+. The results suggest that glial cells in spinal ganglia can respond to depolarizing concentrations of potassium by releasing GABA in a calcium‐dependent process.
EFFECT OF ELECTRICAL STIMULATION ON THE YIELD AND COMPOSITION OF SYNAPTIC VESICLES FROM THE CHOLINERGIC SYNAPSES OF THE ELECTRIC ORGAN OF TORPEDO: A COMBINED BIOCHEMICAL, ELECTROPHYSIOLOGICAL AND MORPHOLOGICAL STUDY
Authors: Zimmermann H. , Whittaker V. P. 
Published: October 2006

Abstract— The effect of stimulating the electric organ of Torpedo marmorata, anaesthetized with 0.01% Tricaine methane sulphonate, by means of electrical stimulation (5/s) administered via an electrode placed on the electric lobe has been studied electrophysiologically, biochemically and morphologically. The response of the organ declined to about 50 per cent of its initial value after about 500 stimuli, by a further 10 per cent after another 500 stimuli and then to about 12 per cent of the initial value after a further 1000 stimuli. Thereafter the response fell off progressively. However, even when the response was less than 1 per cent of its initial value, the organ had considerable powers of recuperation during a 30‐s rest period, to 30–50 per cent of its initial value.The fall in response was accompanied by a reduction in vesicle size and number, an increase in the area of the presynaptic membrane and a fall in the protein, total nucleotide, ATP and acetylcholine content of the vesicle fraction isolated from the stimulated tissue. However, whereas vesicle numbers and the protein and total nucleotide content of the vesicle fraction fell by only about 50 per cent, vesicular ATP and acetylcholine levels were reduced to about 10 per cent. An analysis of the covariance of vesicular ATP and acetylcholine showed an initial loss of an acetylcholine‐rich (relative to ATP) population of vesicles. The early loss of vesicular protein and nucleotide and vesicle numbers as well as the morphological changes seen would be consistent with a loss of vesicles due to fusion with the external membrane. The preferential loss of acetylcholine and ATP from the vesicle fraction indicates that the vesicles surviving the stimulation procedure have been utilized in a number of cycles causing the progressive fall in vesicle volume, and acetylcholine and ATP content.
ACID PROTEINASES AND OTHER ACID HYDROLASES IN EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS: PINPOINTING THE SOURCE1
Authors: Hirsch Hilde E. , Parks Mary E. 
Published: October 2006

Abstract—In Lewis rats with experimental allergic encephalomyelitis (EAE), quantitative histochemical techniques were used to measure the activities of several hydrolytic enzymes, especially acid proteinases, and their levels were correlated with the concentrations of DNA and total lipids. Only those samples which contained lesions (visualized directly or in stained nearby sections) had elevated acid hydrolase activities. A lipase‐esterase hydrolysing a fluorogenic substrate at pH 5.0 was more active in lesions; activity on the same substrate at pH 7.2 was not elevated. β‐Glucuronidase rather than acid proteinase or cathepsin D was the enzyme showing the greatest differences. In a monkey with EAE, studied for comparison, a massive inflammatory lesion appeared to leak β‐glucuronidase to a distance of about 2.5 mm beyond its margin.
GABA CONTENT AND GLUTAMIC ACID DECARBOXYLASE ACTIVITY IN BRAIN OF HUNTINGTON'S CHOREA PATIENTS AND CONTROL SUBJECTS1
Authors: Urquhart Nadine , Perry T. L. , Hansen Shirley , Kennedy Janet 
Published: October 2006

Abstract—GABA contents are significantly decreased in the caudate nucleus, putamen‐globus pallidus, substantia nigra, and occipital cortex in autopsied brain from Huntington's chorea patients, as compared to values in the same regions from control subjects who have died without neurological disease. Homocarnosine levels are lower in choreic than in control brain, but only in the putamen‐globus pallidus and the cerebellar cortex are the differences significant.Activity of the enzyme which synthesizes GABA, glutamic acid decarboxylase, is reduced in the brains of some choreic patients, but may be equally low in brain of control subjects, even though the latter exhibit normal brain GABA content. Low glutamic acid decarboxylase activity in autopsied human brain is not uniquely characteristic of Huntington's chorea.No evidence was found in this study for an inhibitor of glutamic acid decarboxylase in choreic brain, nor for the presence of an isoenzyme with decreased affinity for glutamate. GABA aminotransferase, the enzyme which degrades GABA, was equally active in control and choreic brain; therefore, increased activity of this enzyme cannot account for the low brain GABA levels in Huntington's chorea.
MELANIN FORMATION BY HUMAN BRAIN IN VITRO
Authors: Rodgers A. D. , Curzon G. 
Published: October 2006

Abstract— A quantitative radiometric assay utilising incorporation of 14C from labelled precursors as a measure of melanin formation by human brain in vitro is described. The assay was validated by comparison with various criteria of melanin formation.Catecholamines, DOPA and 5HT were precursors for brain melanin formation. Melanin formation was detected in all brain regions studied and was highest in substantia nigra and striatum.The assay was used to evaluate various hypotheses of brain melanin formation. No evidence for enzymic activity was found and it is concluded that brain melanin formation may be a largely non‐enzymic process.
POSTNATAL CHANGES IN THE POTASSIUM‐STIMULATED, CALCIUM‐DEPENDENT RELEASE OF RADIOACTIVE GABA AND GLYCINE FROM SLICES OF RAT CENTRAL NERVOUS TISSUE
Authors: Davies L. P. , Johnston G. A. R. , Stephanson A. L. 
Published: October 2006

Abstract—Using a simple apparatus designed to perfuse nervous tissue mini‐slices retained on glass fibre filter discs, slices of adult (13 week) rat cerebral cortex and spinal cord were shown to release radioactive GABA and glycine, but not 2‐amino‐isobutyric acid, in response to increased potassium ion concentration of the perfusing medium. A major portion of this potassium‐stimulated release was dependent upon the presence of calcium ions in the perfusing medium. Slices of cerebral cortex and spinal cord from rats of 1 day and 10 days postnatal age showed potassium‐stimulated, calcium‐dependent release of radioactive GABA and glycine respectively. These findings are consistent with other evidence that GABA and glycine are functioning as inhibitory transmitters in rats at least as soon as 1 day after birth.
CARBOHYDRATE AND AMINO ACID METABOLISM IN RAT CEREBRAL CORTEX IN MODERATE AND EXTREME HYPERCAPNIA
Authors: Folbergrová J. , Norberg K. , Quistorff B. , Siesjö B. K. 
Published: October 2006

Abstract—The time course of changes in glycolytic and citric acid cycle intermediates and in amino acids was studied in acute and steady state hypercapnia. Experiments on unanaesthetized animals exposed to 10% CO2 for 10, 20 and 60s showed that there was a transient decrease in glycogen concentration, progressive increases in glucose‐6‐phosphate and fructose‐6‐phosphate and decreases in pyruvate and lactate. During this time the levels of amino acids and Krebs cycle intermediates did not change, except for a small fall in malate at 60s. The results indicate that there was a decrease in glycolytic flux due to an inhibition of the phosphofructokinase reaction. Since the tissue levels of phosphocreatine, ATP, ADP and AMP were unchanged inhibition of phosphofructokinase was probably due to the fall in pH.Anaesthetized animals were exposed to about 5% CO2 (for 2, 5, 15, 30 and 60 min) or to about 45% CO2 (for 5 and 15 min). Except for succinate, which increased, all citric acid cycle metabolites analysed (citrate, α‐ketoglutarate, fumarate and malate) decreased with the rise in CO2‐tension. The sum of the amino acids analysed (glutamate, glutamine, aspartate, asparagine, alanine and GABA) decreased at extreme hypercapnia. The results suggest that Krebs cycle intermediates and amino acids are partly used as substrates for energy production when there is reduced pyruvate availability due to hypercapnia.It is proposed that amino acid carbon is made available for oxidation via transamination (aspartate aminotransferase reaction) and deamination (glutamate dehydrogenase reaction) and that citric acid cycle intermediates are metabolized following a reversal of reactions usually leading to CO2 fixation.
ISOLATION OF HYDROPHOBIC PROTEINS BINDING AMINO ACIDS: γ‐AMINOBUTYRIC ACID BINDING IN THE RAT CEREBRAL CORTEX
Authors: Fiszer de Plazas Sara , Robertis E. De 
Published: October 2006

Abstract—The binding of [14C]GABA to nerve‐ending membranes isolated from rat cerebral cortex follows a hyperbolic curve saturating at 0·4pmol/μg protein. This binding is about 60% inhibited by chloropromazine, and about 40%, inhibited by bicuculline. A hydrophobic protein fraction binding [14C]GABA was separated from the total. lipid extract of nerve‐ending membranes. The binding follows a hyperbolic curve that saturates at 10·5 pmol of [14C]GABA/μg of protein, with an apparent Kd= 30 μm. The binding is competitively inhibited by bicuculline with a Ki= 273 μm. These results are compared with those previously obtained on a GABA binding protein from crustacean muscle.
ALCOHOL:NAD OXIDOREDUCTASE IN BRAIN OF RATS FROM A COLONY FED DILUTE ETHANOL FOR MANY GENERATIONS1,2
Authors: Rodrigo R. , Egaña Enrique 
Published: October 2006

Abstract—Alcohol:NAD oxidoreductase (EC 1.1.1.1) was studied in brain cortex, hypothalamus, cerebellum and midbrain of adult and immature rats, and in the whole encephalon of neonatal rats. The rats used in this study were (i) from a colony which has been given 12% (v/v) aqueous ethanol as the only fluid for 54 generations (‘E.F.’ rats); (ii) rats removed from this colony after the forty‐eighth generation and thereafter fed water instead of the alcohol solution (‘E.F./H2O’ rats); and (iii) normal rats. Enzyme activity in the 20,000 g supernatant of tissue homogenates was measured by the method of Raskin and Sokoloff. Activity was found to be highest in neonatal rat brain and to decrease as the age increased. Activity in the hypothalamus of adult E.F. rats was significantly higher than that found in the same region of adult E.F./H2O rats. Immature rat cerebellum alcohol:NAD oxidoreductase activity was higher both in ‘E.F.’ and ‘E.F./H2O’ suggesting a possible genetic change be involved in this CNS region. It may be concluded that, with the exception of neonatal rats, ethanol consumption induces an increase in rat CNS alcohol :NAD oxidoreductase activity.
THE DISPOSITION OF [24‐3H]CEREBROSTEROL IN DEVELOPING RAT BRAIN*
Authors: Lin Y. Y. , Smith L. L. 
Published: October 2006

Abstract—The uptake into subcellular fractions of developing rat brain in vivo of intracerebrally injected [4‐14C]cholesterol, [24‐3H]cerebrosterol, and [24‐3H]24‐epicerebrosterol was measured for periods up to 30 days following administration. [4‐14C]cholesterol was accumulated rapidly in nuclei, nerve endings, and microsomes, more slowly in myelin and mitochondria. [24‐3H]cerebrosterol was accumulated rapidly in myelin, nerve endings, and microsomes, more slowly in nuclei and mitochondria. The uptake of [24‐3H]24‐epicerebrosterol was essentially the same as that of [24‐3H]cerebrosterol. Ratios of radioactivities of [24‐3H]cerebrosterol and [4‐14C]cholesterol accentuated the early accumulation of [24‐3H]cerebrosterol in myelin, nerve endings, and microsomes, and declining 3H:14C ratios disclosed the rapid elimination of [24‐3H]cerebrosterol and [24‐3H]24‐epicerebrosterol relative to [4‐14C]cholesterol in nerve endings and microsomes. The data suggest that the removal of [24‐3H]cerebrosterol from brain results from an enzymic metabolism of the sterol, therefore that cerebrosterol exists in brain in a dynamic state of biosynthesis and catabolism.
POLYACRYLAMIDE GEL ELECTROPHORESIS OF RAT BRAIN ACETYLCHOLINESTERASE: ISOENZYME CHANGES FOLLOWING PARATHION POISONING1
Authors: Vijayan V. K. , Brownson R. H. 
Published: October 2006

Abstract—Brain acetylcholinesterase (EC 3. 1. 1. 7) isoenzymes of 15‐ and 30‐day‐old rats were found to be inhibited by 2.5 mg/kg and 1.25 mg/kg dosage levels of intraperitoneally administered parathion (E‐605; O, O‐diethyl‐p‐nitrophenyl phosphorothionate). With 2.5 mg/kg dose level, the response of isoenzymes in 15‐ and 30‐day‐old rats was similar. At both ages, there was no significant sex difference in the degree of depression of the isoenzymes.There were no significant regional differences in the degree of inhibition of acetylcholinesterase isoenzymes in the rat brain. At 1.25 mg/kg dosage level, a differential isoenzyme inhibition was evident, with the major isoenzyme (isoenzyme 3) exhibiting the greatest sensitivity to the inhibitor in all brain areas examined.The course of isoenzyme depression and recovery following the administration of parathion differed in brain, serum and skeletal muscle. Whereas brain isoenzymes exhibited most marked inhibition at 2 h after injection, inhibition of serum and skeletal muscle isoenzymes was more prolonged. At 4 h after injection, these isoenzymes were still inhibited while brain isoenzymes had recovered to a substantial degree. Twenty four h following the injection of parathion, when brain and serum acetylcholinesterase isoenzymes had returned to control activity levels, isoenzymes of skeletal muscle demonstrated only minimal recovery.