bluuebunny/crossref_metadata_2025_split huggingface dataset:
LIPID COMPOSITION IN GRAY AND WHITE MATTER OF THE BRAIN IN MENKES' DISEASE
Authors: Lou H. C. , Hølmer Gunhild K. , Reske‐Nielsen Edith , Vagn‐Hansen P. 
Published: October 2006

Abstract— Lipid composition has been determined in brain frontal lobe gray and white matter from a 5‐month‐old patient who died from Menkes' disease, and from a normal control patient of the same age.Total cholesterol and the amount of cholesterol esters were significantly increased in the case of Menkes' disease, whereas the values for free cholesterol were nearly unchanged.In white matter a decrease in total galactolipids was observed in the pathological brain.The values for total phospholipids were unchanged for the tissues, but the ratio between phosphatidylcholines and phosphatidylethanolamines (including ethanolamineplasmalogens) in white matter from the patient seemed increased. The fatty acid pattern of phosphatidylethanolamines (including ethanolamineplasmalogens), phosphatidylcholines and sphingomyelin were similar to those of the normal control. Phosphatidylethanolamines from pathological tissues contained 25–30 per cent polyunsaturated fatty acids with four, five or six double bonds.
RESPIRATION IN IMMATURE RAT BRAIN MITOCHONDRIA
Authors: Holtzman D. , Moore C. L. 
Published: October 2006

Abstract—Respiration was studied polarographically in mitochondria isolated from immature rat cerebral hemispheres. Respiratory rates are compared as a function of age, substrate, and the requirement for a phosphate acceptor.1. All respiratory rates are low in the first week of life. These rates increase during the first month and then decline to about the newborn rate by 5 weeks of age.2. With the NAD‐linked substrate pair, glutamate and malate, the changes with age are significant only for the rate of ADP‐dependent respiration. With succinate as substrate, significant age‐dependent changes in respiration occur only in ADP‐independent respiration.3. In mitochondria from animals less than five weeks of age, the ADP‐dependent respiratory rate is significantly greater with the NAD‐linked substrate pair than with succinate. In mitochondria from older animals, both ADP‐dependent and ADP‐independent rates are greater with succinate.
THE BIOSYNTHESIS OF 3‐METHOXY‐4‐HYDROXYPHENYLGLYCOL SULPHATE BY LIVER AND BRAIN
Authors: Wong K. P. 
Published: October 2006

Abstract—3‐Methoxy‐4‐hydroxyphenylglycol (MHPG) formed a sulphate conjugate when incubated with ATP, Mg2+ ions, Na235SO4 and the high‐speed supernatant preparations of rabbit or rat brain. The same reactions could be catalysed by similar enzyme preparations from liver. The sulphated product was separated and identified by paper chromatography. On acid hydrolysis, it released both Na235SO4 and the free glycol. The measurement of this labelled sulphate was used as a specific assay procedure for determining the overall sulphoconjugatory process. The pH optimum of the reaction is 7.8. For rabbit brain, the Km for Na2SO4 determined for the activating system is 3.6 × 10−4m, and that for MHPG for the sulphotransferase reaction is 1.05 × 10−4m. The specific enzyme activity, expressed as nmol 35SO4 incorporated/h/mg protein for a 30‐min assay is as follows: rat brain, 2.8; rabbit brain, 1.6; rat liver, 33.4and rabbit liver, 15.0. Dithiothreitol at 3 mm concentration had no significant effect on the sulphation of MHPG in all these preparations.
ATPASE AND PHOSPHATIDYLINOSITOL KINASE ACTIVITIES OF ADRENAL CHROMAFFIN VESICLES
Authors: Muller T. W. , Kirshner N. 
Published: October 2006

Abstract— The hypothesis that the ATPase and phosphatidyhnositol (PI) kinase activities of chromaffin vesicle membranes are catalysed by same enzyme was investigated. The two activities exhibited entirely different responses to variations in Mg2+ or Mn2+ concentrations. In the presence of 1 mM ATP, maximal ATPase activity occurred with 1 mM Mg2+ while maximal PI kinase activity required 100 mM Mg2+ Similar differences were observed with Mn2+ with the exception that maximal ATPase activity occurred with 0.5 mM Mn2+ and maximal PI kinase activity occurred with 5 mM Mn2+ Mn2+ was more effective than Mg2+ in stimulating PI kinase activity at low concentrations, but at optimal concentrations of each, the maximal activity obtained with Mg2+ was 5‐fold greater than the maximal activity obtained with Mn2+ The heat stabilities of the two enzymes are vastly different. At 50°C the ATPase activity of the intact membranes was stable for up to 20 min while the tl/2 of PI kinase was less than 2 min. After solubilization in Lubrol PX or at higher temperatures both enzymes were less heat stable, but PI kinase was still inactivated at a much greater rate than the ATPase. The evidence suggests that the ATPase and the PI kinase are different proteins.The major phosphorylated product was diphosphatidylinositol and once formed, it was stable. Phosphorylation of membrane protein accounted for less than 10% of the total 32P‐incorporated into chromaffin vesicles. SDS gel electrophoresis of the solubilized membranes showed the presence of at least 2 major phosphorylated high molecular weight components.
NEURONAL AND GLIAL SYSTEMS FOR γ‐AMINOBUTYRIC ACID METABOLISM
Authors: Sellström Å. , Sjöberg L.‐B. , Hamberger A. 
Published: October 2006

Abstract—Bulk prepared neuronal perikarya, nerve endings and glial cells have been used to study amino acid concentrations and GABA metabolism in vitro. All amino acids were more concentrated in synaptosomes and glial cells than in neuronal perikarya. Cell specificity was found with respect to the relative distribution of some amino acids. Glutamate decarboxylase activity was considerably higher in synaptosomes than in glial cells. The inhibitory effect of amino‐oxyacetic acid on glutamate decarboxylase activity differed between synaptosomes and glial cells. γ‐Aminobutyric acid‐α‐ketoglutarate transaminase had the highest activity in the glial cell fraction; the inhibition of amino‐oxyacetic acid differed between glial and neuronal material. The metabolism of exogenous GABA just accumulated by a cell showed similar time characteristics in neuronal and glial material.
MEMBRANE‐BOUND NEURAMINIDASE IN THE BRAIN OF DIFFERENT ANIMALS: BEHAVIOUR OF THE ENZYME ON ENDOGENOUS SIALO DERIVATIVES AND RATIONALE FOR ITS ASSAY
Authors: Tettamanti G. , Preti A. , Lombardo A. , Suman T. , Zambotti V. 
Published: October 2006

Abstract—The activity of brain membrane‐bound neuraminidase on endogenous and exogenous substrates was comparatively studied in various animals (rat, chicken, rabbit, pig, calf and human). The maximum rate of hydrolysis of endogenous substrates by membrane‐bound neuraminidase (using a crude preparation of the enzyme) was different in the various animals (from 0·05 to 0·73 units, referred to 1 mg protein) and was obtained under similar but not identical optimum conditions (pH from 4·1 to 5·1; requirement or not of Triton X‐100). The maximum degree of hydrolysis of endogenous substates was also different (from 15 to 27 nmol released NeuNAc/mg protein) and was obtained within different incubation periods (from 2 to 18 h). It corresponded (in rabbit, calf, human brain only), or not, to the actual exhaustion of the endogenous substrates.The endogenous substrates were recognized as both gangliosides and sialoglycoproteins. The extent of hydrolysis of sialoglycoproteins varied from 1·5% in rabbit to 15·6% in chicken brain; the hydrolysis of gangliosides (ranging from 14·1% in pig to 53·7% in rabbit brain) reached only in some animals (rabbit, calf, human) the complete transformation of major oligosialogangliosides into the neuraminidase resistant monosialoganglioside GMI. Upon addition of exogenous substrates (sialyl‐lactose, ganglioside GD1a, brain sialopeptides, ovine submaxillary mucin) the actual rate of liberation of total NeuNAc (from both endogenous and exogenous substrates) considerably exceeded, although at a different extent (depending on the animal and on the added substrate used) the rate of hydrolysis of sole endogenous substrates. The possibility of an accurate assay of brain membrane‐bound neuraminidase in a crude enzyme preparation is evaluated and guidelines for the assay procedure suggested.
THE EFFECT OF ASPARTATE ON CITRATE METABOLISM IN THE CYTOSOLIC FRACTION OF BRAIN UNDER CONDITIONS OF NORMOXIA, HYPOXIA AND ANAESTHESIA
Authors: Rafalowska Urszula , Erecińska Maria , Chance B. 
Published: October 2006

Abstract—The utilization of citrate by the cytoplasmic fraction of rat brain is inhibited in hypoxia and remains unaltered in anaesthesia. The addition of exogenous aspartate to the cytosolic fraction isolated from brains of hypoxic animals increases the rate of citrate removal. The level of cytosolic aspartate gradually decreases when the exposure period to low oxygen tension is increased and reaches a minimum after 30 min.The levels of mitochondrial aspartate and of cytoplasmic carbamyl aspartate remain constant. The low level of cytosolic aspartate is accompanied by an increase in the concentration of cytosolic urea and increase in the aspartate level in blood serum. It is suggested that the oxidation of citrate by the cytoplasmic fraction of brain is inhibited in hypoxia owing to the decrease in endogenous aspartate. The decrease in the level of cytoplasmic aspartate is caused by the diversion of this substrate toward urea synthesis and by the increased leakage across the cell/blood barrier to the blood stream. Anaesthesia prevents the changes induced by hypoxia.
CHARACTERIZATION OF POLY(A) SEQUENCES IN BRAIN RNA
Authors: Mahony J. B. , Brown I. R. 
Published: October 2006

Abstract—Nuclear and polysomal brain RNA from the rabbit bind to Millipore filters and oligo(dT)‐cellulose suggesting the presence of poly(A) sequences. The residual polynucleotide produced after RNase digestion of 32P pulse‐labelled brain RNA is 95% adenylic acid and 200‐250 nucleotides in length. After longer isotope pulses the polysomal poly(A) sequence appears heterodisperse in size and shorter than the nuclear poly (A). Poly(A) sequences of brain RNA are located at the 3′‐OH termini as determined by the periodate‐[3H]NaBH4 labelling technique. Cordycepin interferes with the processing of brain mRNA as it inhibits in vivo poly(A) synthesis by about 80% and decreases the appearance of rapidly labelled RNA in polysomes by about 45%. A small poly(A) molecule 10‐30 nucleotides in length is present in rapidly labelled RNA. It appears to be less sensitive to cordycepin than the larger poly(A) and is not found in polysomal RNA.
ACTIONS OF 6‐HYDROXYDOPAMINE QUINONES ON CATECHOLAMINE NEURONS1
Authors: Jonsson G. , Sachs Charlotte 
Published: October 2006

Abstract—The effect of the para‐(PQ) and the ortho‐(OQ) quinones of 6‐hydroxydopamine (6‐OH‐DA) on transmitter uptake‐storage mechanisms of catecholamine neurons in mouse and rat has been investigated. After the administration of PQ and OQ there was a dose‐dependent and long‐lasting disappearance of noradrenaline (NA) nerve terminals as demonstrated by fluorescence histochemistry and a reduction of the in vitro uptake of [3H]NA in mouse atrium and iris. These effects could be completely counteracted by blockade of the ‘membrane pump’ transport mechanism with desipramine, while monoamine oxidase inhibition, by nialamide and administration of ascorbic acid potentiated the effects produced by the two quinones. The results obtained after PQ and OQ were largely identical with those seen after administration of 6‐OH‐DA, well‐known for its neurotoxic action on catecholamine neurons. It is therefore concluded that PQ and OQ are able to produce an acute and selective degeneration of NA nerve terminals similar to that of 6‐OH‐DA. The results obtained after intraventricular injection of the quinones into rat brain were also in agreement with this view. Neonatal administration of PQ or OQ to mice caused a permanent and marked decrease in [3H]NA uptake in the cerebral cortex and the spinal cord, whereas the uptake was markedly increased in the pons‐medulla, similar to that seen after 6‐OH‐DA. The PQ and the OQ were equally potent in most experiments although clearly less potent than 6‐OH‐DA itself. The quinones were also found to be equally or slightly less potent than 6‐OH‐DA in affecting [3H]NA uptake and retention in vitro in atrium and cerebral cortex from untreated mice. It may be concluded that PQ and OQ exert their neurotoxic action on NA neurons after transition to 6‐OH‐DA, after a rapid extraneuronal equilibration. 6‐OH‐DA thus formed can thereafter be taken up and accumulated intraneuronally by use of the ‘membrane pump’ and the specific degenerative action is elicited. The lower neurotoxic potency of the quinones may be attributed to their known ability to undergo covalent binding with proteins and/or formation of 5,6‐dihydroxyindole.
AXOPLASMIC TRANSPORT OF CHOLINE ACETYLTRANSFERASE ACTIVITY IN MICE: EFFECT OF AGE AND NEUROTOMY
Authors: Jablecki C. , Brimijoin S. 
Published: October 2006

Abstract—We studied the axoplasmic transport of choline acetyltransferase (CAT) activity in sciatic nerves of normal mice of various ages. For at least 3 days after unilateral ligation of sciatic nerves of 6 and 30‐week‐old mice, the CAT activity in the ligated nerve increased as a linear function of time and the increase was confined to the 3 mm length of nerve immediately proximal to the ligature. The rate of increase of CAT activity in the ligated nerves of the 30‐week‐old mice was only 45 ± 6% that of the 6‐week‐old mice, whereas the CAT activity of non‐ligated sciatic nerves of the older mice was 87 ± 6% more than that of the younger mice (n = 18, P < 0·001). The average velocity of axoplasmic transport of CAT activity was five times greater in the younger mice (1·5 ± 0·2 mm/day vs 0·3 ± 0·1 mm/day, n = 6, P < 0·01). Even greater differences were observed between still younger and older animals: the av velocity of axoplasmic transport of 2‐week‐old mice (3·5 ± 0·2 mm/day) was 17·5 times greater than that of 36‐week‐old mice (0·2 ± 0·1 mm/day). We also studied the axoplasmic transport of CAT activity in 6‐week‐old mice after unilateral section of the sciatic nerve. For at least 3 months after the operation, there were no differences between the sectioned nerves and the intact contralateral nerves with respect to the increase in CAT activity immediately proximal to a ligature placed at various times after neurotomy and one day before sacrifice. On the other hand, there was a reduction in the CAT activity of more proximal segments of the sectioned nerves. The reduction of CAT activity was maximal (52 ± 3%) 3 weeks after the operation when the maximum increase (2·5‐fold) in the av velocity of axoplasmic transport of CAT activity was recorded (n = 6, P < 0·001). The inclusion of purified (100‐fold) mouse brain CAT activity in the assays for the CAT activity of nerve segments demonstrated that the differences in content and rate of transport were not due to the presence of activators or inhibitors of CAT activity. These differences probably reflect physiologic changes in the axoplasmic transport of cholinergic neurons during development and regeneration.
LONG‐TERM EFFECTS OF TEFLUTIXOL ON THE SYNTHESIS AND ENDOGENOUS LEVELS OF MOUSE BRAIN CATECHOLAMINES
Authors: Hyttel J. 
Published: October 2006

Abstract—The long term effects on accumulation of 14C‐labelled dopamine and noradrenaline after [14C]tyrosine administration and on the endogenous levels of catecholamines in mouse brain were studied after treatment with a new potent thioxanthene neuroleptic, teflutixol. The drug was given as a single dose (5 mg/kg i.p.), as repeated daily doses (1·25 mg/kg p.o.), or as a single dose of the palmitic ester in Viscoleo® (20 mg/kg s.c). After a single dose, teflutixol increased catecholamine synthesis (100%). Noradrenaline synthesis rapidly returned to normal, whereas decreased dopamine synthesis was seen from the third to sixth day, after which it was normal. When the receptors were continuously exposed to teflutixol, either by daily dosage or by the depot preparation, catecholamine synthesis was increased for the first few days but then returned to normal, indicating development of tolerance. Endogenous concentrations of catecholamines were only decreased during the first few days, when the increase in synthesis was greatest. The findings are in accordance with results obtained by Møller Nielsen & Christensen (1975), who found that receptor blockade was followed by receptor supersensitivity after treatment with a neuroleptic compound. The receptor blockade may activate a feedback mechanism that induces increased nervous firing with increased amine synthesis as a consequence. The resulting supersensitivity, if sufficiently great, may lead to reduced nervous firing, followed by slowing of dopamine synthesis.
THE EXCHANGE OF PHOSPHATIDYLCHOLINE AND OF PHOSPHATIDYLINOSITOL IN SHEEP BRAIN
Authors: Brammer M. J. , Sheltawy A. 
Published: October 2006

Abstract—The exchange of phospholipids between liposomes and brain mitochondria has been studied in the presence of pH 5·1 supernatant fluids derived from rat, guinea pig, sheep and ox brains. The exchange phenomenon was similar to that observed in liver and heart, but phosphatidylinositol and not phosphatidylcholine was the most rapidly exchanging phospholipid. The phosphatidylcholine exchange activity was purified 186‐fold from sheep brain and the protein fraction contained two major and several minor protein species. The phosphatidylcholine and phosphatidylinositol exchange activities have been shown to have very similar molecular weights and isoelectric points. However, their behaviour in response to changes in liposomal surface charge suggested that separate proteins might be involved in stimulating the exchange of the two phospholipid classes.
ORGANIC MERCURIAL ENCEPHALOPATHY: IN VIVO AND IN VITRO EFFECTS OF METHYL MERCURY ON SYNAPTOSOMAL RESPIRATION
Authors: Verity M. A. , Brown W. Jann , Cheung M. 
Published: October 2006

Abstract—A reproducible model of subacute methyl mercury (MeHg) intoxication was developed in the adult rat following the daily intragastric administration of 10 mg methyl mercury/kg body wt. Synaptosomes isolated from animals during the latent phase of mercury neurotoxicity (6‐10 days) demonstrated no significant change in respiratory control, State 3, State 4, or 2,4‐dinitrophenol stimulated respiration with succinate, glutamate or pyruvate plus malate. During the neurotoxic phase, a significant decline in respiratory control was evident with all substrates. Cerebellar synaptosomes revealed qualitatively similar but quantitatively greater inhibition of 2,4‐dinitrophenol stimulated respiration during the latent and neurotoxic phases with glutamate. In vitro studies of synaptosome respiration, oxidative phosphorylation and respiratory control with 5‐15 μm‐methyl mercury revealed a stimulation of initial State 4 respiration, loss of RCI, inhibition of State 3 but no change in the gramicidin or 2,4‐dinitrophenol uncoupled rate supported by pyruvate‐malate. Phosphate did not relieve the State 3 inhibition. At 25 μm‐methyl mercury and above, considerable inhibition of electron transfer occurred. At this concentration, cytochrome c oxidase was inhibited 50%. Isosmotic replacement of medium KC1 by mannitol reduced the MeHg stimulation of State 4 respiration but had no effect on MeHg inhibition of ADP stimulated respiration. Half‐maximal stimulation of State 4 respiration by MeHg occurred at [K]+⋍ 6 mm. These findings are compatible with an energy‐linked methyl mercury induced cation translocation across the synaptosome (mitochondrial) membrane.
THE REACTION OF CHOLINE AND 3,3‐DIMETHYL‐1‐BUTANOL WITH THE ACETYLENZYME FROM ACETYLCHOLINESTERASE
Authors: Dawson R. M. 
Published: October 2006

Abstract—A comparison was made of the manner in which choline chloride and 3,3‐dimethyl‐1‐butanol react with the acetylenzyme formed during the hydrolysis of esters of acetic acid by acetylcholinesterase. Acetylcholine and acetylthiocholine were the substrates. The ratio of the formation of alkyl acetate to that of acetic acid increased linearly with the concentration of dimethylbutanol, but approached a limiting value as the concentration of choline was increased. Total enzymic activity was inhibited by choline and activated slightly by dimethylbutanol. The effects of varying ionic strength, pH and substrate concentration were examined. The effects of tetraethyl‐ and tetramethylammonium ions on the reaction of dimethylbutanol with the acetylenzyme were also studied. The results suggest that dimethylbutanol and choline bind to different regions of the active site. A mechanism for the reaction of choline and substrate with acetylcholinesterase is suggested.
CHANGES IN GLYCOGEN PHOSPHORYLASE ACTIVITY AND GLYCOGEN LEVELS OF MOUSE CEREBRAL CORTEX DURING CONVULSIONS INDUCED BY HOMOCYSTEINE
Authors: Folbergrová J. 
Published: October 2006

Abstract—Glycogen phosphorylase activity and glycogen levels were investigated in the cerebral cortex of mice of two different strains under the influence of homocysteine. Control levels of glycogen and total phosphorylase activity (i. e. activity in the presence of 1 mM‐AMP) were higher in the inbred strain A, whereas a higher proportion of phosphorylase in its active form (activity without 5′‐AMP) was obtained in the ICR strain (probably due to slower fixation of brain in this strain). Changes occurring after the administration of homocysteine were similar in both strains. With the onset of first clonic seizures a marked increase of phosphorylase a occurred (increase 99 per cent in strain A and 46.5 per cent in ICR, respectively). During the latter phase of tonic seizures active phosphorylase a did not significantly differ from control values. Five minutes after the end of a tonic seizure, i. e. when partial recovery could already be observed, a marked decrease of active phosphorylase a in comparison with control values, was evident (decrease against control values of 45.5 per cent in strain A and 30.5 per cent in ICR, respectively). The total phosphorylase activity was not affected in strain A, whereas a slight increase during clonic seizures was seen in the ICR strain. In accordance with the enhanced activation of phosphorylase at the onset of clonic seizures, a marked decrease in glycogen levels (35‐50 per cent) was observed in both strains of mice. This decrease persisted even during the 5 min recovery period. When seizures were prevented by Na phenobarbital or glycine, the activation of phosphorylase was either completely prevented (by a non‐anaesthetic dose of phenobarbital) or reduced (by glycine). The present results have demonstrated that changes in glycogen metabolism occurring during homocysteine seizures differ distinctly from those previously found during seizures induced by methionine sulphoximine, a substance structurally related to homocysteine.