bluuebunny/crossref_metadata_2025_split huggingface dataset:
BRAIN LEVELS AND TURNOVER RATES OF PRESUMPTIVE NEUROTRANSMITTERS AS INFLUENCED BY ADMINISTRATION AND WITHDRAWAL OF ETHANOL IN MICE1
Authors: Rawat A. K. 
Published: October 2006

Abstract—Effects of acute or chronic administration of ethanol and its withdrawl on the steady‐state levels and turnover rates of certain neurotransmitters have been investigated in mice. The influence of long‐term administration of ethanol on the activities of enzymes involved in the metabolism of these transmitters has also been studied. Acute administration of ethanol or acetaldehyde or chronic administration of ethanol resulted in a decrease in the cerebral contents of acetylcholine, acetylCoA and CoA. Brain levels of 5‐hydroxytryptamine, norepinephrine and choline remained unchanged after acute administration of ethanol. However, chronic administration of ethanol resulted in a decrease in the norepinephrine content without significantly affecting 5‐hydroxytryptamine or choline contents. Cerebral levels of γ‐aminobutyric acid increased with both acute or chronic administration of ethanol. The total incorporation of [3H]choline into acetylcholine in brain was depressed upon acute administration of ethanol. After withdrawal of ethanol for one day cerebral levels of norepinephrine returned to normal; however, γ‐aminobutyric acid and acetylcholine returned to normal levels at 2 and 4 days after ethanol withdrawal, respectively. Pretreatment of mice with pyrazole, an inhibitor of alcohol dehydrogenase, prevented the ethanol‐induced decrease in cerebral acetylcholine levels. The activities of cerebral choline acetyltransferase and glutamic decarboxylase were decreased after 2 weeks of chronic ethanol administration. However, the activities of acetyl cholinesterase and GABA‐transaminase remained unaffected after 2 weeks of ethanol treatment
PREPARATION AND PROPERTIES OF A CELL‐FREE, HORMONALLY RESPONSIVE ADENYLATE CYCLASE FROM GUINEA PIG BRAIN1
Authors: Chasin M. , Mamrak F. , Samaniego Sylvia G. 
Published: October 2006

Abstract—The accumulation of cyclic adenosine 3′,5′‐monophosphate (cyclic AMP) was studied in cell‐free homogenates of guinea pig brain. Homogenates, prepared in Krebs‐Ringer buffer, responded markedly to the addition of neurohormones with an increased rate of cyclic AMP synthesis; preparations from cerebellum, cerebral cortex, and hippocampus responded to a degree approximating that achieved with slices of these areas of guinea pig brain. Adenylatc cyclase activity was seen only when cyclic AMP was measured by a [3H]adenine prelabelling technique or when total cyclic AMP was measured by radioimmunoassay; [32P]ATP did not serve as a substrate for this preparation of the enzyme. The adenylate cyclase was paniculate and required a Krebs Ringer buffer; use of tris, or tris with Mg2+ and Ca2+, resulted in a preparation totally devoid of hormonal stimulation. Digestion by purified beef heart cyclic nucleotide phosphodiesterase, Dowex chromatography, solubility in Ba(OH)2‐ZnSO4 mixtures, and two thin layer chromatographic systems demonstrated that the product of the hormonally stimulated adenylate cyclase preparation was cyclic AMP. The selectivity of hormonal stimulation and the adrenergic character of the hormonal receptors from different brain areas were maintained in the cell‐free preparation. However, simultaneous stimulation with two different neurohormones resulted in additive responses, rather than in the potentiation observed in preparations of slices of brain.
PHOSPHOLIPID METABOLISM IN EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS: ACTIVITY OF MITOCHONDRIAL PHOSPHOLIPASE A2 OF RAT BRAIN TOWARDS SPECIFICALLY LABELLED 1,2‐DIACYL‐, 1‐ALK‐1′‐ENYL‐2‐ACYL‐ AND 1‐ALKYL‐2‐ACYL‐SN‐GLYCERO‐ 3‐PHOSPHORYLCHOLINE
Authors: Woelk H. , Kanig K. , Peiler‐Ichikawa K. 
Published: October 2006

Abstract—1,2‐Diacyl‐, 1‐alk‐1′‐enyl‐2‐acyl‐and 1‐alkyl‐2‐acyl‐sn‐glycero‐3‐phosphorylcholine, specifically labelled with different fatty acids at the 2 position, were prepared enzymically using the acyltransferase system of rabbit sarcoplasmic reticulum. The substrates were submitted to hydrolysis by mitochondrial phospholipase A2 (phosphatide acyl‐hydrolase, EC 3.1.1.4) obtained from normal and from rat brain afflicted with EAE. In the acute stage of the disease an increase of approximately 25 per cent in phospholipase A 2 activity could be observed in comparison to that from the control animals for all investigated substrates. Phospholipase A2 obtained from normal rat brains and from those afflicted with EAE had a higher affinity for 1,2‐diacyl‐sn‐glycero‐3‐phosphorylcholine when compared to the corresponding alkyl acyl‐ and alkenyl acyl‐analogues. Choline plasmalogen was cleaved more slowly than the corresponding alkyl acyl derivative. The enzyme activity returned to the control level in the recovery stage of the demyelinating disease.
LABELLING OF ACETYLCHOLINE IN THE BRAIN OF MICE FED ON A DIET CONTAINING DEUTERIUM LABELLED CHOLINE: STUDIES UTILIZING GAS CHROMATOGRAPHY—MASS SPECTROMETRY
Authors: Hanin I. , Schuberth J. 
Published: October 2006

Abstract—A method to achieve labelling of the acetylcholine stores of the brain under ideal physiological conditions is described. To this end, mice fed on a choline free diet were supplied with deuterium labelled choline in the drinking water. Labelled and unlabelled choline in plasma and in the brain as well as labelled and unlabelled acetyicholine in the brain were measured by a gas chromatographic‐mass spectrometric method. It was found that after 1–25 days on the deuterium choline diet, substantial amounts of the plasma choline and brain acetylcholine were displaced by deuterium choline and deuterium acetylcholine, respectively. Already on the first day, the mole ratio of deuterium choline/total choline in plasma was 0·22, and it approached a maximum of 0·57 on the 14th day. The mole ratios of deuterium acetylcholine/total acetylcholine in the brain were slightly but significantly lower than those of deuterium choline/total choline in plasma 1–14 days, but asymptotically approached the mole ratios of deuterium Ch/total Ch in plasma by 25 days. Intact brains submitted to incubation at room temperature for 10 min increased their total choline content by about 500 per cent. Concurrently, in brains from animals kept on a deuterium choline diet for 1–2 days, the level of deuterium choline rose only by 50 per cent after incubation. Deuterium choline levels increased, however, by 200–300 per cent in the brains from animals kept on the deuterium diet for longer time periods.On the basis of these data it is suggested that: (a) choline in plasma is partly supplied from the food and partly from endogenous sources; (b) plasma choline rapidly equilibrates (less than one day) with a pool of Ch in the brain which is responsible for biosynthesis of acetylcholine; (c) the size of this choline pool is in the order of 34–40 nmol/g.
ACTIONS OF NEUROHUMORAL AGENTS AND CEREBRAL METABOLITES ON OUTPUT OF ADENINE DERIVATIVES FROM SUPERFUSED TISSUES OF THE BRAIN
Authors: Pull I. , McIlwain H. 
Published: October 2006

Abstract—Adenine nucleotides of guinea‐pig neocortical tissues were labelled by prior incubation with [14C]adenine and excess of adenine was then removed by superfusion with precursor‐free media. During continued superfusion labelled adenine derivatives were released at a stable rate of about 0·05 per cent of the tissue 14C/min and this rate was increased about five‐fold by electrical stimulation. Various compounds, including some known to increase the cyclic AMP content of cerebral tissues, were examined for action on the release of [14C]adenine derivatives from the tissue and also on the rates of lactate production by the tissue, both before and during electrical excitation. The tissue content of adenine nucleotides following exposure of the tissue to these compounds was also determined.Noradrenaline, γ‐aminobutyrate and acetylcholine together with carbamoylcholine at the concentrations examined were without effect on the release of 14C compounds from the tissue. Also, noradrenaline and γ‐aminobutyrate caused no alteration in lactate production but brought about some decrease in the adenylate energy charge of the tissue. Histamine, 100 μm, brought about a small but consistent increase (35 per cent) both in release of 14C‐compounds and lactate output, while reducing the adenylate energy charge of the tissues. l‐Glutamate at 5 mm decreased the tissue adenylate energy charge to a greater extent than did histamine; it increased the release of 14C‐compounds seven to eight‐fold and similarly increased the tissues' rates of lactate production. Lower concentrations of glutamate had smaller effects. In those cerebral tissues whose cyclic AMP content is increased by l‐glutamate, the increase is probably brought about by intermediation of released adenosine.
THE SUBCELLULAR DISTRIBUTION OF β‐PHENYLETHYLAMINE, p‐TYRAMINE AND TRYPTAMINE IN RAT BRAIN
Authors: Boulton A. A. , Baker G. B. 
Published: October 2006

Abstract—The quantitative subcellular distribution of β‐phenylethylamine, p‐tyramine and tryptamine in rat brain was investigated using the mass spectrometric integrated ion current technique. More of the total cellular tryptamine was found to be associated with paniculate fractions than was the case for phenyiethylamine and p‐tyramine but a significant amount of this tryptamine was found to be labile. Analysis of the particulate fractions indicated that each of the amines was localized predominantly in the crude P2 pellet and that the bulk of this was associated with the synaptosomal (P2B) fraction. Inhibition of monoamine oxidase systems with pargyline caused an increase in the level of all three amines in all fractions, but the increase was greater in the supernatant than in the combined particulate fractions. This treatment produced changes in the distribution of β‐phenylethylamine and p‐tyramine between the various particulate subcellular fractions but did not markedly alter the distribution of tryptamine between the same fractions.
ACETYLCHOLINESTERASE TURNOVER IN BRAIN, CEREBROSPINAL FLUID AND PLASMA
Authors: Yaksh T. L. , Filbert M. G. , Harris L. W. , Yamamura H. I. 
Published: October 2006

Abstract—By assay of acetylcholine hydrolysis to measure total cholinesterase activity and acetyl‐β‐methylcholine hydrolysis to measure acetylcholinesterase (E.C 3.1.1.7) activity, patterns of regeneration of enzyme activity were measured in seven areas of brain, cerebrospinal fluid and plasma of cats after administration of an irreversible inhibitor. Halftimes of recovery of total cholinesterase in the brain tissues ranged from 0·9 to 3·8 days (av = 2·5 days) and acetylcholinesterase recovery halftimes ranged from 1·2 to 5·3 days (av = 3·6 days).Regeneration of total cholinesterase was also followed in subcellular fractions of guinea‐pig and rat brains after similar inhibition. In both species, the fastest recovery occurred in the soluble fraction with halftimes of 1·8 and 1·6 days, while the synaptosomal fractions exhibited the slowest recoveries with halftimes of 8·3 and 4·1 days. Regeneration of activity in plasma and CSF most nearly resembled that of the soluble brain fraction.
PUTATIVE TRANSMITTERS IN DENERVATED OLFACTORY CORTEX
Authors: Harvey J. A. , Scholfield C. N. , Graham L. T. , Aprison M. H. 
Published: October 2006

Abstract—Olfactory bulb removal and the consequent degeneration of the lateral olfactory tract led to a selective change in putative synaptic transmitters of the denervated olfactory cortex of guinea‐pigs. Nine days after bulbectomy there was a significant decrease in content of aspartate (31%) and glutamate (20%) in olfactory cortex but no change in neocortex. The content of GABA, alanine and ACh in olfactory cortex was unchanged (± 3 per cent of control). The content of 5‐HT, dopamine, NE and glycine was increased by 10‐18 per cent. The decrease in aspartate and glutamate content of the olfactory cortex after bulbectomy suggests that these two amino acids have a high concentration in fibres of the lateral olfactory tract. This tissue may prove to be useful in determining the possible role of these acidic amino acids in neuronal function.
EFFECT OF DIETARY PROTEIN AND CALORIE DEFICIENCY ON TRYPTOPHAN LEVELS IN THE DEVELOPING RAT BRAIN
Authors: Kalyanasundaram S. 
Published: October 2006

Abstract—The pattern of development of brain tryptophan in the rat was studied in the progeny of mothers fed a 7.5%; protein diet ad lib., a 20% protein diet ad lib. and those fed a 20%; protein diet pair‐fed with mothers who received the 7.5% protein. The pattern of development was similar in all three groups. Starting with a high brain tryptophan content at birth, all animals showed a progressive reduction during the next 3 weeks. However, tryptophan levels at birth were several fold higher in the brains of pups born to mothers receiving either the low protein diet fed ad lib. or those born to mothers who received the 20% protein diet in restricted amounts. From the 14th day after birth, tryptophan concentration of brain in undernourished pups was significantly lower until the 35th day. The implications of this finding are discussed.
THE MOTOR END‐PLATE SPECIFIC FORM OF ACETYLCHOLINESTERASE: APPEARANCE DURING EMBRYOGENESIS AND RE‐INNERVATION OF RAT MUSCLE
Authors: Vigny M. , Koenig Jeanine , Rieger F. 
Published: October 2006

Abstract– We have solubilized three active molecular forms of AChE from rat muscle and have confirmed the presence of one of these forms (EP form, apparent sedimentation coefficient: 16 s) uniquely at the motor end‐plate regions of several skeletal muscles. This form was never detected in smooth muscle extracts. In sternocleidomastoïdian muscle it disappeared after denervation and reappeared after re‐innervation in the region where nerve and muscle had come in contact. During the embryonic development of hind leg muscles the EP form appeared on the 14th or 15th day of gestation.The EP form of muscle AchE appears to be an excellent biochemical marker of the neuromuscular junction.
CHANGES IN THE CEREBRAL METABOLISM INDUCED BY HYPER VENTILATION AT DIFFERENT BLOOD GLUCOSE LEVELS
Authors: Norberg K. 
Published: October 2006

Abstract—In order to study cerebral metabolism in hypocapnia, lightly anaesthetized rats were hyperventilated to PaCO2 about 15 mm Hg for 1, 2, 5 and 30min, the brain was frozen in situ, and cortical concentrations of organic phosphates, glycolytic and citric acid cycle metabolites, and amino acids were measured. In separate experiments, animals were made hypoglycaemic prior to induction of hypocapnia. Measurements of arteriovenous differences for oxygen and glucose indicated an increased glycolytic flux and the pattern of changes in glycolytic intermediates after 1 min suggested that this was due to an activation of the phosphofructokinase step.The pool size of citric acid cycle intermediates gradually increased with time of hypocapnia. This increase was, as in hypoxic hypoxia, related to the accumulation of pyruvate, probably via its effect on the alanine aminotransferase reaction and on the rate of CO2 fixation at the pyruvate carboxylase step. In hypoglycaemic, hypocapnic animals, in which the production of pyruvate was limited, the increase in pool size did not occur. It is suggested that the pyruvate concentration determines the net flux at the CO2 fixation step and thereby the direction of net flux of carbon skeletons between the citric acid cycle and the glycolytic chain. The changes in amino acids (glutamate, glutamine, alanine, GABA and aspartate) with time of hypocapnia were also similar to those occurring in hypoxic hypoxia. Thus, there was an increase in alanine concentration and a shift in aspartate aminotransferase reaction with increase in glutamate and fall in aspartate. It is suggested that the increase in alanine was secondary to a rise in pyruvate concentration, and that the shift in the aspartate aminotransferase reaction was due to reduction of the malate dehydrogenase system. This interpretation is supported by the fact that hypoglycaemia, by preventing a rise in pyruvate concentration and a reduction in the cytoplasmic redox system, also prevented the changes in amino acids.
INTRACRANIAL CONVERSION OF LINOLEIC ACID TO ARACHIDONIC ACID: EVIDENCE FOR LACK OF Δ8 DESATURASE IN THE BRAIN
Authors: Dhopeshwarkar Govind A. , Subramanian Carole 
Published: October 2006

AbstractEleven‐day old rats were given intracranial injection of [1‐14C]linoleic acid (all cis 9,12 octadecadienoic acid) and sacrificed after 8 h. Analysis of brain fatty acids showed that 16:0, 18:2, 20:2,20:3 and 20:4 were labeled. Separation by AgN03:Si02 TLC plates followed by reductive ozonolysis characterized thc polyunsaturated fatty acids as 18:2 (Δ9,12), 20:2 (Δ11,14), 20:3 (Δ8,11,14) and 20:4 (Δ5,8,11,14). A smaller amount of 18:3 (Δ6,9,12) was also identified. This initially suggested 20:2 (A1 1,14) as an intermediate in the optional pathway of biosynthesis of arachidonate. However, when [l‐14C]eicosadienoic acid (Δ1 1,141 itself was injected in the brain it was converted to 20:3 (Δ5,11,14) (a non‐methylene interrupted double bond system) rather than the expected 20:3 (Δ8,11,14). Only a small amount of arachidonate was formed from 20:2 (Δ11,14). Thus it was concluded that 20:2 (Δ11,14) was not an intermediate in the pathways of arachidonate biosynthesis due to lack of Δ5 desaturase in thc brain which agrees with the findings of SPKECRER & LEE (1975) in rat liver.
PROPERTIES OF THE EXTERNAL ACETYLCHOLINESTERASE IN GUINEA‐PIG IRIS
Authors: Karlsen R. Lund , Fonnum F. 
Published: October 2006

Abstract— The acetylcholinesterase (AChE) of intact iris, the so‐called external AChE, differs in several respects from the AChE in an homogenate of iris, called the total AChE. Maximum enzyme activities of the external and total AChE were obtained with an ACh concentration of 10 and 1.3 mm, respectively. The total AChE exhibited substrate inhibition at high substrate concentrations, whereas the external enzyme did not exhibit substrate inhibition in the range studied. The external AChE activity, when measured at 1.3 mm‐ACh. accounted only for 12% of the total enzyme activity. After irreversible inhibition of AChE with diisopropylfluorophosphate (DFP) or methylisocyclopentylfluorophosphate (soman) the external AChE recovered to almost normal values after 48 h, whereas only 30% of the total AChE recovered during this period. Pupillographic studies after inhibition with DFP demonstrated that pupillary diameter had reached normal size after 24 h.Destruction of the cholinergic input to iris reduced the total AChE activity by 40%, but did not alter the external AChE activity nor its rate of recovery after DFP inhibition. The specific activities of total AChE and total choline acetyltransferase were significantly higher in the sphincter than in the dilator muscle. After such denervation of iris the greatest reduction in total AChE and choline acetyltransferase were found in the sphincter region. After treatment with DFP the total AChE was inhibited to the same extent and recovered at the same rate in both regions.After extraction of AChE from iris with various salt solutions and detergents, the particulate enzyme recovered faster than the soluble enzyme from DFP inhibition.
UPTAKE OF GLUCOSE ANALOGUES BY RAT BRAIN CORTEX SLICES: MEMBRANE TRANSPORT VERSUS METABOLISM OF 2‐DEOXY‐d‐GLUCOSE
Authors: Lund‐Andersen H. , Kjeldsen Christel S. 
Published: October 2006

Abstract— —The uptake of the glucose analogue 2‐deoxy‐d‐glucose by rat brain cortex slices was studied in order to compare the rate of membrane transport with the rate of phosphorylation in the concentration range 5–12 mM‐glucose plus 0.5–15 mM‐2‐deoxy‐glucose. The comparison was carried out by fitting a model of the brain slice to uptake data and by determination of 2‐deoxy‐glucose and 2‐deoxy‐glucose‐6‐phosphate by ion exchange chromatography.The rate of membrane transport exceeded the rate of phosphorylation by at least one order of magnitude. The membrane transport was so rapid that the extracellular diffusion became rate limiting for the uptake. The membrane transport could therefore only be determined as a minimum value and it was not possible to determine unidirectional flux across the cell membranes (initial rate). Accordingly, characterization of the membrane tranport with respect to maximal transport rate and affinity was not possible. The phosphorylation reaction, however, was so slow that it was accessible for exact determination and only the phosphorylation reaction was responsible for the fact that the cellular uptake of 2‐deoxy‐glucose was of the Michaelis‐Menten type, thus emphasizing the importance of dissociation between membrane transport and metabolism when transport is studied of a substance which can undergo metabolism.The data indicate that glucose transport across glial and neuronal membranes is not rate limiting for glucose metabolism of brain tissue in vitro.
STUDIES ON RAT SPINAL CORD POLYSOMES: POSTNATAL DEVELOPMENT AND EXPERIMENTAL DEMYELINATION1
Authors: Chiu Fung‐Chow , Smith Marion Edmonds 
Published: October 2006

AbstractSpinal cord polysomes were prepared from 15‐day‐old rats, 3‐month‐old rats, and adult triethyl tin‐fed and control rats by a procedure adapted from that of Zomzely‐Neurathet al. (1973) for brain polysomes. The state of aggregation and the activity in a cell‐free system supplemented with a hepatic enzyme fraction were studied with these preparations. The properties of the amino acid‐incorporating system in spinal cord polysomes were similar to those of brain systems with respect to rapid incorporation in the first 30 min of incubation, dependence on polysomes and supplementary enzymes, sensitivity to emetine and high Mg2+, and relative insensitivity to cycloheximide. Polysomes from 15‐day‐old rats were more highly aggregated than those from 3‐month‐old rats, but incorporation of radioactive amino acids was not different in the preparations from the two age groups with respect to the requirement for the supplementary enzyme fraction or the kinetics. Spinal cord polysomes prepared from rats with chronic triethyl tin‐induced edema and demyelination were slightly more aggregated than those from the controls. Average increases of 30% in amino acid incorporating activity were observed in spinal cord polysomes from triethyl tin‐fed rats compared to those of controls. Similar increases have been shown previously in fractions from the spinal cord slice, especially in the myelin fraction (Smith, 1973). Spinal cord polysomes from rats in two stages of development and in different experimentally‐caused physiological states behaved differently within the limits of our in vitro system.
NIEMANN PICK DISEASE: PRESENCE OF THE MAGNESIUM‐DEPENDENT SPHINGOMYELINASE IN BRAIN OF THE INFANTILE FORM OF THE DISEASE1
Authors: Gatt S. , Dinur T. , Kopolovic J. 
Published: October 2006

Abstract— Brain of a 14‐month‐old patient with the infantile form of Niemann Pick disease was found to be practically devoid of sphingomyelinase activity when assayed at pH 5. When assayed at pH 7.4, in the presence of magnesium ions considerable hydrolysis of sphingomyelin was obtained by brain preparations. The rate of hydrolis of a homogenate of grey matter was about 0.3 μmol. mg protein−1. H−1, corresponding to about 15 μmol of sphingomyelin hydrolysed perg brain in 1 h.The possibility is suggested that the presence of the extra‐lysosomal, magnesium dependent sphingomyelinase in brain of Niemann Pick patients may be responsible, in part, for the lesser accumulation of sphingomyelin in this tissue relative to other organs, such as liver or spleen.