bluuebunny/crossref_metadata_2025_split huggingface dataset:
A TECHNIQUE FOR MEASURING BRAIN PROTEIN SYNTHESIS
Authors: Garlick P. J. , Marshall I. 
Published: October 2006

Abstract— Mice were infused intravenously for varying periods of time with L‐[U‐14C]‐ tyrosine. The specific activity of free tyrosine in the blood and the brain, and of protein‐bound tyrosine in the brain, was measured and the mean rate of protein synthesis calculated. The half‐life of mixed brain proteins was found to be close to 4 days with infusions lasting 0.5–2 h.The origin of the intracellular tyrosine pool was investigated and it was shown that 60 per cent of this was derived directly from the plasma tyrosine and 40 per cent from protein breakdown within the tissue.
THE PRESENCE OF BIOLOGICALLY LABILE COMPOUNDS DURING ISCHEMIA AND THEIR RELATIONSHIP TO THE EEG IN RAT CEREBRAL CORTEX AND HYPOTHALAMUS
Authors: Swaab D. F. , Boer K. 
Published: October 2006

Abstract—Two surgical methods are described in the present paper, allowing for the approximate determination of in vivo levels of ATP, lactate, glucose, pyruvate and glycogen in anatomically uninjured cortex and hypothalamus from unanaesthetized rats. It was not possible to obtain such levels for P‐creatine in the 2 mm thick samples used in the present investigation. No fundamental difference was observed between the cortical and the hypo‐thalamic levels of these substrates nor in their fluxes.The substrate fluxes during ischemia were correlated with electrical activity in the rat cortex and hypothalamus, recorded by means of telemetrically transmitted electroencephalograms. The electrical activity declined precipitously at 9.6 s after decapitation in the cortex, and after 12.1 s in the hypothalamus. High levels of glycogen, glucose and ATP were present at this moment, while P‐creatine had declined sharply.
THE EFFECT ON GABA METABOLISM IN BRAIN OF ISONICOTINIC ACID HYDRAZIDE AND PYRIDOXINE AS A FUNCTION OF TIME AFTER ADMINISTRATION
Authors: Wood J. D. , Peesker S. J. 
Published: October 2006

Abstract—The effect of intramuscularly administered INH on brain levels of GABA in chicks was dependent on the amount injected. A subconvulsant dose of INH (1·1 mmol/kg) produced a slow steady decline in the level of GABA, whereas a convulsant dose (2·19 mmol/kg) brought about a sequential fall and rise in GABA level. This sequence of events reflected changes in the relative activities of GAD and GABA‐T brought about by the hydrazide. The administration of pyridoxine together with the INH (2·19 mmol/kg) prevented the onset of seizures and lessened the effect of the INH on GABA levels and GAD activity but not on GABA‐T activity. The possibility that a deranged GABA metabolism is responsible for hydrazide‐induced seizures is discussed.
REMOVAL AND UTILIZATION OF KETONE BODIES BY THE BRAIN OF NEWBORN PUPPIES
Authors: Spitzer J. J. , Weng J. T. 
Published: October 2006

AbstractThe removal of circulating ketone bodies by the brain was investigated in 0‐ to 8‐day‐old puppies under pentobarbital anaesthesia. Of the arterial acetoacetate (AcAc) and β‐hydroxybutyrate (βOHB), 24 and 30 per cent, respectively, were removed by the brain. There was a direct correlation between the arterial concentrations of either AcAc or βOHB and the A‐V difference of the respective ketone body across the brain. When a continuous infusion of Na‐dl‐3‐hydroxybutyrate [3‐14T] was administered for more than 2 h, labelling of both phospholipids and free cholesterol was consistently observed in all six areas of the brain that were sampled. We conclude that the removal and utilization of ketones is of physiological importance in the brain of newborn animals.
TEMPERATURE AND INHIBITOR EFFECTS ON FAST AXONAL TRANSPORT IN A MOLLUSCAN NERVE
Authors: Heslop J. P. , Howes Elizabeth A. 
Published: October 2006

Abstract—The cerebro‐visceral connective of Anodonta cygnea has been shown to provide a convenient system for experiments on fast axonal transport. The transport mechanism is directional, independent of the cell bodies, inhibited by cyanide, dinitrophenol and colchicine but is resistant to anoxia. Although the rate of transport increases with temperature above 15°C it is more or less temperature‐independent from 4 to 15°C, i.e. over the normal temperature range of this pond‐dwelling mollusc.
LIPID COMPOSITION OF QUAKING MOUSE MYELIN: COMPARISON WITH NORMAL MOUSE MYELIN IN THE ADULT AND DURING DEVELOPMENT1
Authors: Baumann N. , Bourre J. M. , Jacque C. , Harpin M. L. 
Published: October 2006

Abstract— In the ‘Quaking’ mouse, a deficiency in the long chain fatty acid content of galactolipids has been shown to occur.Myelin in the mutant has been compared to myelin in adult and in 12‐day‐old controls. We have shown that myelin is not only quantitatively reduced but also qualitatively modified, with a higher protein and a lower galactolipid content. Cerebrosides contain only a small amount of kerasin, lacking long chain nonhydroxylated fatty acids in comparison to both controls; the relative percentage of phrenosin is increased.Although many similarities exist between adult Quaking myelin and myelin at 12 days, differences have been shown to occur which may be in relation to a genetic block at an earlier stage of development.
Extractability of glycoproteins and mucopolysaccharides of brain
Authors: Margolis R. K. , Margolis R. U. 
Published: October 2006

Very little is known about the localization and functions of the glycoproteins and mucopolysaccharides of nervous tissue. There have been two major approaches to the study of these substances in brain. The first involves the isolation of glycopeptides and mucopolysaccharides after digestion of the lipid‐free protein residue from whole brain with proteolytic enzymes (Margolis, 1967; Di Benedettaet al., 1969; Margolis and Margolis, 1970; Katzman, 1972). This approach has the advantage that sufficient tissue is used to permit analysis of the structure and metabolism of the carbohydrate components of these macromolecules. However, any differentiation of the various glycoproteins and mucopolysaccharides based on such features as their anatomical location, association with proteins, lipids or other membrane components, and the properties conferred by their non‐carbohydrate portion, is unavoidably lost as a consequence of the procedures used for their isolation.On the other hand, several laboratories have attempted to study the glycoproteins and mucopolysaccharides of nervous tissue by treating brain (or subcellular fractions) with various detergents, and then examining the extracts for the pattern of separation obtained by polyacrylamide gel electrophoresis in terms of carbohydrate staining reactions or the incorporation of labelled precursors (Bosmann, Case and Shea, 1970; Duiton and Barondes, 1970; Quarles and Brady, 1971; Waehneldt, Morgan and Gombos, 1971). This approach has the advantages of relatively high sensitivity and the ability to study intact glycoproteins rather than glycopeptides produced by proteolytic enzyme digestion. However, it is presently impossible to identify any of the numerous and often poorly resolved bands thus obtained with glycoproteins or mucopolysaccharides of known structure and chemical composition, or in many cases even to identify the various complex carbohydrates as being glycoproteins, glycolipids or acid mucopolysaccharides.In an attempt to obtain some indication of the degree of anatomical heterogeneity of these compounds in nervous tissue, we have sequentially treated whole rat brain with several solvents to obtain intact glycoproteins and mucopolysaccharides. After removal of lipids and digestion with pronase, the composition of the glycopeptides and mucopolysaccharides has been analyzed.
BIOSYNTHESIS OF CHOLEST‐5‐ENE‐3β, 24‐DIOL (CEREBROSTEROL) BY BOVINE CEREBRAL CORTICAL MICROSOMES1
Authors: Dhar A. K. , Teng J. I. , Smith Leland L. 
Published: October 2006

AbstractThe presence of cholest‐5‐ene‐3β, 24‐diol (cerebrosterol) in samples of human, bovine, and rabbit brains has been established by isolation of the sterol therefrom and identification by comparison of physical properties. Cholest‐5‐ene‐3β, 24‐diol was present at the level of 66.5 sg/g of dried tissue in human brain, 42.9 μg/g in cattle brain, and 89.5 pg/g in rabbit brain. Cholest‐5‐ene‐3β, 24‐diol was the only readily detectable hydroxycholesterol derivative in these brain tissues and was concentrated in the 105,000 g pellet (microsomal fraction) of both human and bovine cerebral cortex, with no demonstrable amounts of the sterol present in nuclear or mitochondrial fractions. Incubation of [1,2‐3H]‐ or of [4‐14C]‐cholesterol with the 105,000 g microsomal pellet from bovine cerebral cortical homogenates demonstrated 0.1‐0.38 per cent conversions to radioactive cholest‐5‐ene‐3β, 24‐diol, isolated and purified as the 3β, 24‐dibenzoate. The bioconversion required oxygen, and a stimulation of hydroxylation by added NADPH2 was demonstrated. Our observations establish that a sterol 24‐hydroxylase system is present in bovine cerebral cortex.
EFFECTS OF ACETYLCHOLINE ON THE IN CORPORATION OF [32P]ORTHOPHOSPHATE IN VITRO INTO THE PHOSPHOLIPIDS OF SUBSYNAPTOSOMAL MEMBRANES FROM GUINEA‐PIG BRAIN
Authors: Yagihara Y. , Bleasdale J. E. , Hawthorne J. N. 
Published: October 2006

Abstract‐Synaptosomes prepared from guinea‐pig cerebral cortex were incubated with 32P1 in a medium with or without 10−4 M‐acetylcholine and 10−4 M‐eserine. They were then subjected to osmotic shock and density‐gradient centrifugation for the preparation of subsynaptosomal fractions and the phospholipids of each fraction were separated by two‐dimensional thin‐layer chromatography.The fraction containing synaptic vesicles and that containing mitochondria were the most highly labelled of the sub‐synaptosomal fractions. Phosphatidic acid followed by phosphatidylinositol had the highest specific activity of the phospholipids studied. Acetylcholine caused a marked increase in the specific activity of the vesicular but not of the mitochondrial phosphatidic acid. Phosphatidylinositol specific activity also increased in the presence of acetylcholine but the increase was more reproducible in the fraction containing microsomal membranes than in the vesicle fraction. The other phospholipids were relatively poorly labelled and no effect of acetylcholine on the incorporation of 32P1 into these lipids could be detected. Acetylcholine also caused a decrease in the amount of phosphatidic acid in the synaptic vesicles.
EXPERIMENTAL MATERNAL HYPERPHENYLALANINEMTA: DISAGGREGATION OF FETAL BRAIN RIBOSOMES
Authors: Copenhaver J. H. , Vacanti J. P. , Carver M. J. 
Published: October 2006

AbstractDisaggregation of polyribosomal structures has been demonstrated in fetal rat brains following treatment of the maternal animal with para‐chloro‐d,l‐phenylalanine (used primarily to inhibit maternal phenylalanine hydroxylase, EC 1.14.3.1) and with phenylalanine (used to raise the level of circulating phenylalanine in maternal and fetal plasma). Since highly disaggregated polyribosomal systems cannot support normal levels of protein synthesis in vitro, it has been postulated that the composition of the free amino acid pool(s) plays a regulatory role in protein synthesis through the intermediary effect of polyribosomal aggregation‐disaggregation. We believe that a possibly prolonged period of disaggregation of neuronal polyribosomes might disrupt neuronal protein synthesis sufficiently in utero to produce the mental insufficiency observed in the offspring of untreated maternal phenylketonurics.
ACCUMULATION AND METABOLISM OF NOREPINE‐PHRINE IN RAT HYPOTHALAMUS AFTER EXHAUSTIVE STRESS1
Authors: Stone E. A. 
Published: October 2006

Abstract—Exhaustive stress in rats is followed by a temporary reduction of hypothalamic norepinephrine (NE) together with a persistent increase in turnover during recovery. To test for persistent alterations of NE storage and metabolism produced by stress, rats were subjected to 3 h of forced running and were then injected intraventricularly with [3H]NE or [3H]dopamine (DA). The hypothalamus was assayed for [3H]NE and its metabolites at various intervals after injection. The effects of stress were compared with those of reserpine (7·5 mg/kg) or α‐methyltyrosine (AMT, 300 mg/kg) pretreatment. It was found that the stress‐induced reduction of endogenous NE was not accompanied by a change in the accumulation of exogenous [3H]NE either 10 or 30 min after injection, whereas the NE depletions produced by reserpine or AMT were associated with decreased or increased accumulation, respectively. However, stress did produce an increased accumulation of [3H]NE endogenously synthesized from [3H]DA. These results indicate that exhaustive stress does not adversely affect the storage of NE. They also suggest that stores of NE depleted by stress are replenished chiefly with newly synthesized NE and not through an increased uptake and binding or decreased metabolism of extraneuronal NE. The latter factors may play a role in the maintenance of brain NE stores when biosynthesis is low, i.e. after AMT. The major metabolites of exogenous [3H]NE, at 30 min after injection, were identified as conjugates of 3,4‐dihydroxyphenylglycol (DOPEG) and 3‐methoxy‐4‐hydroxyphenylglycol (MOPEG) in approximately equal amounts. The finding of high levels of conjugated DOPEG confirms a recent report (Slgden and Eccleston, 1971) that this compound is a major metabolite of brain NE. Reserpine produced marked elevations of both conjugates; AMT slightly reduced each. Prior stress increased only conjugated MOPEG, an observation suggesting that CNS levels of this metabolite may reflect NE released by nervous activity.
SIALIC ACID INCORPORATION INTO GANGLIOSIDES AND GLYCOPROTEINS OF THE FISH BRAIN1
Authors: Rösner H. , Wiegandt H. , Rahmann H. 
Published: October 2006

Abstract—The concentration of lipid‐ and non‐lipid‐bound sialic acid in the optic nerve tract and tectum and in whole brain of fish was estimated. The incorporation of sialic acid into gangliosides and non‐lipid components was studied in fish by intracranial or intraocular application of N‐[3H]acetylmannosamine or N‐[3H]acetylglucosamine. After intracranial injection of N‐[3H]acetylmannosamine autoradiography showed lipid‐ and non‐lipid‐bound radioactivity in the tectum opticum evenly distributed over regions of nerve fibres or perikarya indicating an ubiquitous incorporation of label. Sialic acid incorporation into glycoproteins after intracranial injection of N‐acetylmannosamine always exceeded that into gangliosides. TCA‐precipitable non‐lipid material is labelled from intracranially applied N‐acetylmannosamine in the sialic acid portion and also in nonsialic acid components, whereby the percentage of label in sialic acid increases reaching 90 per cent of the total radioactivity after 90 min. After intraocular application of N‐[3H]acetylmannosamine, sialic acid in gangliosides was generally found to be more highly labelled than in glycoproteins. The ratio of radioactivity in gangliosides and glycoproteins increased with time of incubation and the distance from the eye. TCA‐soluble radioactivity was translocated by fast axonal transport. Cycloheximide inhibited incorporation of N‐acetylmannosamine‐derived radioactivity into gangliosides and proteins but not the transport of TCA‐soluble material, which accumulates in the tectum. After intraocular application of N‐[3H]acetylglucosamine, TCA‐soluble label arrives later in the optic tectum than radioactivity of high molecular weight components. The ratio of lipid to non‐lipid‐bound radioactivity does not change considerably with the time after injection or the distance from the eye. There was no accumulation of TCA‐soluble radioactivity after the inhibition of incorporation into high molecular weight components.
AN ASSAY PROCEDURE FOR TRYPTAMINE IN BRAIN AND SPINAL CORD USING ITS [3H]DANSYL DERIVATIVE
Authors: Snodgrass S. R. , Horn A. S. 
Published: October 2006

Abstract—The tryptamine content of rat and mouse brain and spinal cord was determined with a radiochemical derivative assay, using [3H]dansyl chloride. The amine was extracted into toluene‐isoamyl alcohol, back‐extracted into dilute acid, then adsorbed onto a non‐ionic polystyrene resin, and dansylated in tetrahydrofuran after elution from the resin. Optimum recoveries were obtained with TCA extracts, although significant losses occurred due to surface adsorption and protein binding. The brain content of tryptamine increased after MAO inhibition and was not significantly further increased when tryptophan loading was combined with inhibition of MAO and/or tryptophan 5‐hydroxylase. The tryptamine concentration of spinal cord exceeded that of brain and increased rapidly after death. Among brain regions tryptamine concentrations were greatest in hypothalamus and striatum and lowest in cerebral cortex and cerebellum.
CHANGES IN CENTRAL NORADRENALINE NEURONSADMINISTRATION AFTER SYSTEMIC 6‐HYDROXYDOPAMINE ADMINISTRATION
Authors: Sachs Charlotte , Jonsson Gösta 
Published: October 2006

Abstract—Intravenous injection of a large dose of 6‐hydroxydopamine (100 mg/kg) to adult rats caused a significant and long‐lasting reduction (about 30 per cent) of the in oirro uptake of [3H]NA in the cerebral cortex and spinal cord, while no changes were seen in the hypothalamus. The endogenous NA in whole brain was similarly reduced (about 20 per cent). Fluorescence histochemistry revealed catecholamine accumulations which are degenerative signs, induced by 6‐hydroxydopamine, in axons of the dorsal NA bundle innervating the cerebral cortex. It is concluded that the blood–brain barrier in adult rats is not completely protective with respect to the neurotoxic action of systemically injected 6‐hydroxydopamine, which can produce degeneration of a significant number of NA nerve terminals in the cerebral cortex and spinal cord. Previous studies have shown that 6‐hydroxydopamine caused a permanent and selective degeneration of a large number of central NA nerve terminals when injected systemically up to 1 week after birth, due to an incompletely developed blood‐brain barrier. This barrier for 6‐hydroxydopamine develops between the 7th and 9th day after birth (Sachs, 1973). In the present study 6‐hydroxydopamine was found to cause a small transient reduction in [3H]NA uptake in cerebral cortex of rats between 9 and 28 days of age, while in older rats the damage produced by 6‐hydroxydopamine was long‐lasting. Thus, the NA nerves ascending to the cerebral cortex seem to possess a regenerative capacity to a 6‐hydroxydopamine‐induced degeneration up to about 28 days postnatally, but which later disappears or is markedly retarded.
THE EFFECT OF THIAMINE DEFICIENCY ON THE ACETYLCOENZYMEA AND ACETYLCHOLINE LEVELS IN THE RAT BRAIN
Authors: Heinrich C. P. , Stadler H. , Weiser H. 
Published: October 2006

Abstract—It is shown that transketolase activities in red blood cells and whole brain of normal and thiamine‐deficient rats correlate well with heart frequencies.The effect of thiamine depletion on the levels of acetylcoenzyme A (acetyl‐CoA) and acetylcholine (ACh), and on the activities of pyruvate dehydrogenase, choline acetyl‐transferase and acetylcholine esterase was studied in whole brains of thiamine‐deficient, thiamine‐supplementedad libitumand pair‐fed rats. The concentrations of acetyl‐CoA and ACh decreased in thiamine‐deficient brains by 42 and 35 per cent, respectively.Total pyruvate dehydrogenase activity did not change during vitamin B1deficiency. The ‘resolved’ enzyme, reconstituted with thiamine diphosphate, had an association constant of 5.4 × 10−6m. Choline acetyltransferase and acetylcholine esterase activities remained unchanged in thiamine deficiency.Possible mechanisms which could explain the reduced Ach levels in vitamin B1deficiency are discussed.
NORADRENALINE NERVE TERMINALS IN THE CEREBRAL CORTEX: EFFECTS ON NORADRENALINE UPTAKE AND STORAGE FOLLOWING AXONAL LESION WITH 6‐HYDROXYDOPAMINE
Authors: Lidbrink P. , Jonsson G. 
Published: October 2006

AbstractThe ascending noradrenaline‐containing neuronal system from the locus coeruleus to the cerebral cortex was unilaterally lesioned by an intracerebral injection of 8 μg 6‐hydroxydopamine in the dorsomedial reticular formation in the caudal mesencephalon. The 6‐hydroxydopamine caused injury to axons of the dorsal catecholamine bundle associated with its specific neurotoxic action, while very limited unspecific tissue necrosis was observed.Following this treatment the endogenous noradrenaline in the ipsilateral cerebral cortex (neocortex) increased acutely (up to 2 days), as observed both with noradrenaline assay and fluorescence histochemistry. The noradrenaline concentration then gradually decreased to 15 per cent of the contralateral side 15 days after the lesion. At this time interval and up to at least 90 days no fluorescent catecholamine nerve terminals could be detected. The acute noradrenaline increase could be blocked partially by tyrosine hydroxylase inhibition produced by α‐methyl‐p‐tyrosine. The disappearance of endogenous noradrenaline following tyrosine hydroxylase inhibition was also reduced after the 6‐hydroxydopamine lesion.Studies on the in vitro uptake of [3H]noradrenaline (0.1 μM for 5 min) in slices from the neocortex after the 6‐hydroxydopamine lesion showed a gradual decline in uptake reaching maximal reduction (35‐40 per cent of the contralateral side) after 15 days. No recovery of [3H]noradrenaline uptake was seen up to 90 days after the lesion. The formation of [3H]noradrenaline from [3H]dopamine in vitro was reduced to 15 per cent of the contralateral side after a chronic lesion.The present results indicate that the disappearance of noradrenaline uptake‐storage mechanisms in the neocortex is due to an anterograde degeneration of axons and nerve terminals of the dorsal catecholamine bundle. The data on endogenous noradrenaline and noradrenaline synthesis suggest that approx. 15 per cent of the noradrenaline nerve terminals in the neocortex remain intact following the lesion, while the [3H]noradrenaline uptake data reflect uptake in other tissue structures in addition to noradrenaline nerve terminals, e.g. dopamine nerve terminals, pericytes and/or glial cells.