bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE ONTOGENY OF DOPAMINE‐DEPENDENT INCREASE OF ADENOSINE 3′,5′‐CYCLIC MONOPHOSPHATE IN THE CHICK RETINA
Authors: De Mello F. G. 
Published: October 2006

AbstractThe adenosine 3′,5′‐cyclic monophosphate level of chick embryonic retina changes during the course of development. In retinas from 6‐ to 15‐day‐old embryos the cAMP level is approximately 7 pmol/mg protein. A sharp 3‐fold increase is observed between the 16th and 18th embronic day and remains constant thereafter. A dopamine‐dependent increase in cAMP of the chick retina is already present in 7‐day‐old embryos, and by the 8th embryonic day maximal response is attained. Glutamate promotes a 2‐fold stimulation. Carbachol, γ‐aminobutyric acid and glycine do not cause any significant change in the level of cAMP of the embryonic tissue.Guanosine 3′,5′‐cyclic monophosphate also accumulates during development. Its concentration is approx 0.5 pmol/mg protein from the 8th to the 14th embryonic day, then increases gradually until the 19th day of development when the level observed is approx 14 pmol/mg protein.
DNA‐DEPENDENT RNA POLYMERASES FROM RAT BRAIN, AND RNA SYNTHESIS IN GLIAL AND NEURONAL CELL‐ENRICHED FRACTIONS, AFTER PROTEIN RESTRICTION
Authors: Kubaat.G. Birgitta , Morean Marianne , Decken Alexandra von der 
Published: October 2006

AbstractDNA‐dependent RNA polymerases were extracted from rat brain and separated by column chromatography on DEAE Sephadex into enzyme I and II. After 6 days of dietary protein restriction the α‐amanitin sensitive RNA polymerase II showed a decrease in activity per total brain wet weight, and per mg brain DNA. RNA polymerase I was unchanged under these conditions. The acid‐soluble pool of nucleotides was also unaffected. Separation of brain tissue into glial‐ and neuronal‐enriched cells revealed dietary effects on RNA synthesis in glial but not in neuronal elements.Brain wet weight and DNA content remained unaltered after 6 days of protein restriction: but body weight was reduced by 1.3 g day. Control rats increased in weight by 7.7 g/day.
BIOCHEMICAL CHARACTERIZATION OF THE NEURON: RIBONUCLEIC ACID COMPOSITION OF THE NEURONAL CELL BODIES
Authors: Okazaki Hiroko , Abe Sachiko , Satake Mei 
Published: October 2006

AbstractBase composition of the two major RNA species, 18 S and 28 S, from the neuron were determined. Bulk isolation of the neuronal cell bodies, acrylamide gel electrophoresis of RNA and the microelectrophoresis of the hydrolysate of RNA species were carried out successively for this purpose. It is revealed that 28 S RNA has a base composition which resembles those reported for the cerebral cortex and other tissues. The base composition of the 18 S RNA from the neuron, however, differs from cerebral cortex and other tissue base compositions in that the neuronal 18 S RNA contains a higher percentage of C and a lower percentage of G compared with other tissues.
ENHANCED CEREBRAL PROTEIN SYNTHESIS IN DEVELOPING HYPOTHYROID RATS: EVIDENCE FOR DELAYED MATURATION
Authors: Gonzales Linda W. , Geel Stanley E. 
Published: October 2006

Abstract(1) Neonatal hypothyroidism resulted in a 40% increase in the incorporation of [14C]leucine into protein by cerebral cortical slices from 25‐day‐old rats. The uptake of the [14C]‐labelled amino acid into the acid‐soluble free amino acid pool was similar in hypothyroid and control groups which excluded the possibility that transport differences contributed to the observed differences in incorporation. (2) The conversion of [14C]leucine in the free amino acid pool to other metabolites was substantially greater in the hypothyroid state compared to euthyroid controls. (3) The correction of the incorporation data for radioactivity associated with [14C]leucine in the precursor pool, provided an estimate of cerebral protein synthetic rate which was markedly higher in thyroid hormone‐deficient‐rats compared to litter mate controls. (4) The administration of L‐thyroxine to hypothyroid animals for two successive days essentially returned the accelerated metabolism of the precursor pool leucine to normal but failed to ameliorate the increased incorporation into protein. (5) Incubations conducted in the presence of high exogenous leucine levels, to eliminate possible differences in intracellular free amino acid pool size, provided additional evidence for an increased rate of cerebral protein synthesis in 25‐day‐old hypothyroid rats compared to controls. (6) The results are compatible with a retardation in the normal developmental decline in the rate of cerebral protein synthesis associated with hypothyroidism.
IDENTIFICATION AND QUANTIFICATION OF 3‐METHOXY ‐4‐HYDROXYPHENYLLACTIC ACID (VLA) IN CEREBROSPINAL FLUID AND 3‐METHOXY‐4‐HYDROXY PHENYLPYRUVIC ACID (VPA) IN THE URINE OF PARKINSONIAN PATIENTS TREATED WITH L‐DOPA
Authors: Muskiet F. A. J. , Jeuring H. J. , Teelken A. W. , Wolthers B. G. , Lakke J. P. W. F. 
Published: October 2006

AbstractThe identification and quantification of 3‐methoxy‐4‐hydroxyphenyllactic acid in cerebrospinal fluid, and 3‐methoxy‐4‐hydroxyphenylpyruvic acid in the urine of Parkinsonian patients on medication with l‐3,4‐dihydroxyphenylalanine with or without a peripheral decarboxylase inhibitor are described. Data are also given for other catecholamine‐ and catecholamine precursor metabolites in urine and cerebrospinal fluid. Analyses were performed by means of gas chromatography with flame ionization or mass spectrometric detection. We have concluded that following the administration of l‐3.4‐dihydroxyphenylalanine + peripheral decarboxylase inhibitor. 3‐methoxy‐4‐hydroxyphenyllactic acid must be considered as a quantitatively important metabolite of L‐3.4‐dihydroxyphenylalanine in cerebrospinal fluid. In addition, some comment is given on the presence of 3‐methoxy‐4‐hydroxy‐phenylpyruvic acid in the urine of these patients.
PRODUCTS OF BIOGENIC AMINE METABOLISM IN THE LOBSTER: SULFATE CONJUGATES
Authors: Kennedy Mary B. 
Published: October 2006

Abstract—Octopamine, dopamine and serotonin, the three biogenic amines found in the lobster nervous system, are each converted by lobster tissues into two principal classes of products, A and B metabolites. In this paper, evidence is presented that the B metabolites are sulfate conjugates of the amines and their A metabolites. Two double‐labelled conjugates were formed from each of the three amines during incubations of lobster nerves with tritiated amine and 35SO4. When the two octopamine conjugates were hydrolyzed by mild acid, one of the conjugates was converted to a mixture of 35SO4 and [3H]‐octopamine, and the other to a mixture of 35SO4, [3H]octopamine, and [3H]metabolite A. [3H]Metabolite A was also converted to octopamine by acid hydrolysis. The results indicated that one of the double‐labelled conjugates was octopamine‐sulfate, and the other metabolite‐A‐sulfate. An enzyme fraction prepared from nerve homogenates catalyzed the synthesis of double‐labelled sulfate conjugates from the tritiated amines and [35S]3′‐phosphoadenosine‐5′‐phospho‐sulfate. Double‐labelled conjugates formed in this way contained 1 mol of sulfate per mol of amine. Indirect evidence suggested that the sulfate was in ester linkage with the ring hydroxyls of the amines.Neither monoamine oxidase, nor catechol‐O‐methyl transferase is found in lobster tissues; therefore, in these animals, sulfation may be a major means of inactivation of the biogenic amines following their release from nerve endings.
MEASUREMENT OF ACETYLCHOLINE TURNOVER WITH GLUCOSE USED AS PRECURSOR: EVIDENCE FOR COMPARTMENTATION OF GLUCOSE METABOLISM IN BRAIN
Authors: Gibson Gary E. , Blass John P. , Jenden Donald J. 
Published: October 2006

Abstract—The turnover of acetylcholine in whole mouse brain in vivo has been determined using [U‐14C]glucose as a precursor of the acetyl moiety. The standard requirements for the measurement of turnover were met: the injection did not change the concentrations of precursor or product, the amount of radioactivity in the brain was proportional to the amount injected, and the relationship between the specific activity of glucose and that of acetylcholine was typical of a precursor and a product. The value for acetylcholine turnover was 64 pmol/min per mg protein, approx 6.4 nmol/min per g brain. Treatment with amobarbital (0.16 mmol/kg) decreased the incorporation of glucose into acetylcholine by 73 × 7%, and treatment with atropine increased it by 18 × 6%. These values agree with those using choline as a precursor, supporting the validity of the values for turnover obtained with either labelled precursor.The specific activity of acetylcholine was higher than that of pyruvate at all times in mouse brain in vivo and in rat brain slices in vitro. These observations demonstrate compartmentation of glucose metabolism with respect to acetylcholine synthesis in the brain. They agree with observations by others of compartmentation of acetyl metabolism. They provide an explanation for the close linkage which has been observed between carbohydrate catabolism and acetylcholine synthesis in the CNS.
STUDIES ON NICOTINIC ACETYLCHOLINE RECEPTORS IN MAMMALIAN BRAIN. CHARACTERIZATION OF A MICROSOMAL SUBFRACTION ENRICHED IN RECEPTOR FUNCTION FOR DIFFERENT NEUROTRANSMITTERS
Authors: de Blas Angel , Mahler Henry R. 
Published: October 2006

Abstract— A subfraction, derived from the microsomal fraction of rat cerebral cortex, with a buoyant density of 1.112 g μ ml−1 appears to be enriched in receptor sites for a number of potential neurotrans‐mitters. These include the cholinergic (nicotinic and muscarinic) and ß‐adrenergic receptors. This microsomal subfraction (P3B2) has been isolated on a preparative scale by two sequential isopycnic sedimentations in discontinuous sucrose gradients.We have studied the morphology, enzymatic markers and protein composition of this fraction and have compared them with the properties of other subcellular fractions from the same source. Synaptic plasma membranes resembled P3B2 by exhibiting the same high extent of enrichment in receptors. However, the synaptic membranes appear to contain more mitochondrial and presynaptic (axonal and cell surface) membranes than does P3B2, and the postsynaptic membranes in the two fractions appear morphologically distinct since P3B2 does not contain the characteristic postsynaptic densities. Thus these membranes may be derived from Gray's type II synapses.
ACTIVE UPTAKE OF [3H]5‐HT BY SYNAPTIC VESICLES FROM RAT BRAIN
Authors: Halaris Angelos E. , DeMet Edward M. 
Published: October 2006

Abstract—The question of whether synaptic vesicles accumulate [3H]5‐HT by an active process was investigated in a mixed population of vesiclcs from whole rat brain. The temperature dependence and the effect of metabolic inhibitors were studied in synaptosomal suspensions and vesicular fractions. Arrhenius plots for synaptosomes differed from those for vesicles as did the temperature coefficients for these two fractions. For synaptosomes the Q10 was 7 and for vesicles 1.6. However, if ATP was added to the incubation, the temperature dependence of vesicular amine accumulation became manifest; the Arrhenius plot resembled that of synaptosomes and the Q10 was greater than 20 indicating strong temperature dependence. In the presence of ATP, vesicular uptake was stimulated approx 8‐fold. Ouabain, dinitrophenol and NEM inhibited synaptosomal uptake but failed to affect [3H]5‐HT accumulation by vesicles in the absence of ATP. When ATP was added, vesicular uptake was also blocked by NEM but was unaffected by either ouabain or DNP. Total observed uptake consisted of two components, one ATP‐dependent and one nonsaturable and ATP‐independent. The active process had a Km= 1.25 × 10−7 M and could be completely blocked by either 10−3 M or 10−7 M‐reserpine. Active vesicular [3H]5‐HT uptake was magnesium dependent and was inhibited by sodium and potassium. Cation effects on uptake were specific and could not be accounted for by either changes in osmotic pressure or ionic strength. It was concluded that synaptic vesicles from whole rat brain accumulate [3H]5‐HT by an active process.
CYCLIC AMP‐DEPENDENT PROTEIN KINASE ACTIVITY AND SYNAPTOSOMAL PROTEIN PHOSPHORYLATION IN THE BRAINS OF AGED RATS
Authors: Schmidt Michael J. , Truex Lewis L. , Conway Richard G. , Routtenberg Aryeh 
Published: October 2006

Abstract—The activity of soluble protein kinase and phosphorylation of endogenous synaptosomal proteins were studied in vitro, in the hippocampus and cerebral cortex of rats 3, 12, or 24 months of age. No between‐age differences in the activity of cyclic AMP‐dependent or independent protein kinase were detected in either brain region. The degree of stimulation by cyclic AMP and the apparent Ka, for cyclic AMP were similar at all stages. Cyclic AMP stimulated the phosphorylation of synaptosomal proteins from the cerebral cortex, hippocampus, caudate nucleus, and cerebellum of rats at all ages. There were no significant differences across age in the extent of phosphorylation of any membrane proteins in any brain region. The number and staining density of synaptosornal proteins separated by polyacrylamide gel electrophoresis were also similar at all ages. These studies indicate that the cyclic AMP‐dependent phosphorylation system in the rat brain does not change during advanced aging.
A BIOCHEMICAL‐BEHAVIORAL MODEL FOR STUDYING SEROTONERGIC SUPERSENSITIVITY IN BRAIN
Authors: Fleisher L. N. , Simon J. R. , Aprison M. H. 
Published: October 2006

AbstractChronic treatment with p‐chlorophenylalanine methylester (PCPA) resulted in enhanced sensitivity to D,L‐5‐hydroxytryptophan (5‐HTP) induced inhibition of response rates in rats working on a Variable Interval 1 min schedule of milk reinforcement. Marked depletions of 5‐hydroxytryptamine (5‐HT) were found in the cerebral cortex, hippocampus, striatum, diencephalon, mesencephalon, and pons‐medulla oblongata. Much smaller dopamine depletions were seen in some areas, particularly the hippocampus and pons‐medulla oblongata. Analysis of the binding of [3H]5‐HT to crude membrane fractions from the cerebral cortex of PCPA‐treated animals indicated a significant decrease in the apparent dissociation constant (KdAPP) for 5‐HT, but no change in the maximum binding capacity. The increased behavioral sensitivity to 5–HTP does not seem to be due to increased conversion of 5‐HTP to 5‐HT, increased uptake of 5‐HTP, or release of 5‐HT by p‐chlorophenylethylamine. However, the possibility that p‐chlorophenylalanine or the metabolite p‐chlorophenylacetic acid increased the binding of 5‐HT, thus decreasing KdAPP, cannot be ruled out. Some parallels between a recently proposed model of human depression and the observations of the present investigation are discussed.
INHIBITION OF BRAIN GLUTAMATE DECARBOXYLASE BY 2‐KETO‐4‐PENTENOIC ACID, A METABOLITE OF ALLYLGLYCINE1
Authors: Reingold Diane F. , Orlowski Marian 
Published: October 2006

Abstract— 2‐Keto‐4‐pentenoic acid, a potent inhibitor of brain glutamate decarboxylase (Orlowskiet al., 1977) was prepared by oxidative deamination of l‐allylglycine with snake venom l‐amino acid oxidase. In the presence of glutamate the keto acid is a competitive inhibitor of the enzyme with respect to glutamate; its Ki is 2.4 ± 10−6m. After preincubation of brain glutamate decarboxylase with 2‐keto‐4‐pentenoic acid in the absence of glutamate, a slow and incomplete reactivation is obtained by prolonged dialysis, Sephadex gel‐filtration, and dilution, suggesting the formation of a slowly dissociating enzyme‐inhibitor complex and partial inactivation of the enzyme. In vivo inhibition of brain glutamate decarboxylase after administration of allylglycine is maximal after 2‐8 h with activity returning to normal after 16 h. The inhibition of the enzyme after administration of d‐allylglycine was greatest in the cerebellum and the medulla‐pons area, the sites of the highest activity of d‐amino acid oxidase. These results are interpreted as strongly supporting the postulate that allylglycine‐induced inhibition of brain glutamate decarboxylase is due to the in vivo formation of 2‐keto‐4‐pentenoic acid.
CHEMICAL SYNTHESIS OF [3H]CEREBROSIDE [35S]SULFATE AND ITS IN VIVO METABOLISM IN RAT BRAIN
Authors: Nonaka Genichiro , Kishimoto Yasuo 
Published: October 2006

Abstract—Double‐labeled sulfatide containing [3‐3H]lignoceric acid and [35S]sulfate was synthesized and injected intracerebrally into 28‐day‐old rats. The 3H‐labeled sulfatide was synthesized by condensing (RS)‐[3‐3H]lignoceroyl chloride with lysosulfatide which had been obtained by saponification of sulfatide. The 35S‐labeled sulfatide was synthesized by using [35S]sulfuric acid for sulfating 2′, 4′, 6′‐tri‐benzoyl‐galactosyl N‐fatty acyl, N‐benzoyl‐3‐0‐benzoyl‐sphingosine, which had been obtained by per‐benzoylation followed by solvolysis of calf brain nonhydroxycerebrosides. The perbenzoylated [35S]sul‐fatide was then subjected to mild alkaline saponification. Eight hours following the injection, the brain lipids contained various radioactive sphingolipids in addition to sulfatides. Fourteen per cent of the injected 3H was recovered in total lipids, and 26% of this was found in sulfatide. Nonhydroxy‐ and hydroxyceramides, nonhydroxy‐ and hydroxycerebrosides, and polar lipids contained 7, 1, 8, 3, and 22 per cent of the 3H found in total lipids, respectively. On the other hand, only 6% of the 35S injected was recovered in total lipids; 63% of this was found in sulfatide, 5% in a mixture of seminolipid and cholesterol sulfate and 10% in a water‐soluble material.
A ROLE FOR MICROTUBULES IN THE REGULATION OF 3‐HYDROXY‐3‐METHYLGLUTARYL COENZYME A REDUCTASE AND CHOLESTEROL BIOSYNTHESIS IN CULTURED GLIAL CELLS 1
Authors: VOLPE J. J. 
Published: October 2006

Abstract—Cultured C‐6 glial cells were utilized to evaluate the effect of the antimicrotubular drug, Colcemid, on 3‐hydroxy‐3‐melhylglutaryl coenzyme A (HMG‐CoA) reductase and cholesterol synthesis in cultured C‐6 glial cells. The data indicate that Colcemid causes a marked inhibition of cholesterol synthesis (from [14C]acetate or 3H2O) in these cells. A concentration of 0.5 μM led to a 50% lower rate of synthesis after 2 h and an 80–85% lower rate after 12 h or longer. That the effect of Colcemid is mediated at the level of HMG‐CoA reductase was shown by defining closely coordinate temporal and quantitative changes in the activity of this enzyme under identical conditions. No comparable change in cell growth or in total protein synthesis accompanied the effect of Colcemid. The drug did lead to a decrease in the rate of DNA synthesis (from [3H]thymidine) but this effect was preceded by the decrease in the rate of cholesterol synthesis. Marked changes in glial cell shape were induced by exposure to Colcemid, and the temporal and quantitative aspects of these changes appeared to closely parallel the effects on reductase activily and cholesterol synthesis.The dala suggest that microtubules are involved in the regulation of HMG‐CoA reductase and cholesterol synthesis in mammalian cells and that there are important interrelations between microtubules, glial differentiation and cholesterol synthesis.
ADDENDUM TO A NEW MATHEMATICAL APPROACH TO METABOLISM OF [14C]GLUCOSE: THE PYRUVATE CARBOXYLASE REACTION 1
Authors: Larrabee Martin G. 
Published: October 2006

Abstract—Previously published equations for analysis of [14C]glucose metabolism assumed that products of glycolysis enter the citric acid cycle only through acetyl‐CoA (Larrabee, 1978). These equations are now extended to include entrance into the citric acid cycle through the pyruvate carboxy‐lase reaction as well as via acetyl‐CoA and are applied to previously reported data from dorsal root ganglia of 15‐day‐old chicken embryos. The rate of output of labelled CO2 in the presence of [2‐14C] glucose could not be accounted for if the flux rate into the citric acid cycle through the pyruvate carboxylase reaction was assumed to be more than about 10–15% of that through acetyl‐CoA. It is concluded (1) that the pyruvate carboxylase reaction is a relatively minor source of material for the citric acid cycle in these ganglia and (2) that the previous conclusions about [14C]glucose metabolism, which ignored the pyruvate carboxylase reaction, need not be modified in the light of this reanalysis.
ALTERATIONS IN THE BINDING OF [3H]LEUCINE‐ENKEPHALIN TO STRIATAL MEMBRANES BY ENDOGENOUS FACTORS
Authors: Rothman Richard B. , Westfall Thomas C. 
Published: October 2006

Abstract—Saturation binding studies with [3H]leu‐enk ([tyrosyl‐3, 5‐3H(N)]5leu‐enkephalin) revealed the presence of high and low affinity binding sites in a paniculate fraction derived from rat striatum. The binding of [3H]leu‐enk to the high affinity component (KD= 2.0 ± 0.3 nM) was sensitive to morphine and levorphanol, while the binding to the low affinity component (KD= 21 ± 2 nM) was not.Incubation of the membranes, prior to assay for 30 min at 37°C, followed by centrifugation at 27, 000 g for 20 min in order to pellet the membranes allowed the detection of a factor, present in the high speed supernatant, which caused a dose‐dependent inhibition of the binding of [3H]leu‐enk to the morphine‐sensitive and insensitive binding components.Investigations into the nature of the morphine‐insensitive binding component demonstrated that it was an artifact since it was not detectable when bound and free ligand were separated by centrifugation. Furthermore, [3H]leu‐enk bound to Whatman glass fiber filters, used to collect bound ligand, in a morphine‐insensitive manner, and under conditions where the binding of [3H]leu‐enk to the morphine sensitive component diluted proportionally with serial dilutions of the membranes, the binding to the morphine‐insensitive component did not.The factor present in the high speed supernatant did not dialyze and its effects were mimicked by either trypsin or soybean trypsin inhibitor, but not by bovine serum albumin.The apparent inhibition of the binding of [3H]leu‐enk to these binding components is probably not of biological significance, but the fact that the artifactual morphine insensitive binding component of striatal membranes has been shown to decrease by 20–30% following lesions of the substantia nigra suggests that the influence of this endogenous factor must be controlled for.
ATP‐Dependent Ca2+ Accumulation by Microvesicles Isolated from Bovine Neurohypophyses
Authors: Torp‐Pedersen Christian , Særmark Torben , Bundgaard Magnus , Thorn Niels A. 
Published: October 2006

Abstract: Microvesicles with and without coats were isolated from bovine neurohypophyses by a series of ultracentrifugation steps. They were similar to microvesicles previously isolated from brain. In the presence of ATP and Mg2+, the microvesicles accumulated calcium. Oxalate stimulated and the Ca2+ ionophore A23187 inhibited calcium accumulation. In the presence of Ca2+ and Mg2+ the microvesicles also demonstrated ATPase activity. As judged by SDS electrophoresis in polyacrylamide gels microvesicle protein composition was very different from that of neurosecretory granules, suggesting that they are not granule membranes “retrieved” after exocytosis. They may have an important function in regulation of Ca24 ion concentration.