bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECTS OF INSULIN AND STREPTOZOTOCIN–NDUCED DIABETES ON BRAIN TRYPTOPHAN AND SEROTONIN METABOLISM IN RATS
Authors: Mackenzie R. G. , Trulson M. E. 
Published: October 2006

Abstract—Previous work by other authors has shown hat insulin administration increases brain tryptophan levels and serotonin (5–HT) metabolism. The present study partially replicates these results and tests whether these effects could be due to insulin‐induced hypoglycemic stress, since stressers such as immobilization or food deprivation also increase brain tryptophan and 5‐HT metabolism. Ingestion of a dextrose solution by rats administered insulin (2 I.U./kg) prevents the extreme fall in blood glucose concentration and rise in plasma corticosterone following insulin injections alone. This treatment, however, produces a larger increase in brain tryptophan (30%) than insulin‐injected rats allowed only tap water. The greater accumulation of brain tryptophan may reflect an additive effect of the endogenously released insulin to that exogenously administered, since ingestion of the dextrose solution could trigger insulin secretion. In addition, brain tryptophan and 5‐HT metabolism were measured in streptozotocin‐diabetic rats maintained on several different feeding schedules to control for the effects of hyperphagia. All groups of diabetics showed significant decreases of approx 30% in brain tryptophan concentrations, while 5‐HT metabolism was unchanged. This deficit in brain tryptophan is reversed within 2 h after insulin administration (2 I.U./kg). These results indicate that changes in brain tryptophan and 5‐HT metabolism following insulin injections are not due to hypoglycemic stress, and that brain tryptophan is low in diabetics but increases above normal after administration of insulin. The results are discussed with respect to the effects of insulin on plasma levels of the neutral amino acids and a possible direct effect of insulin on the uptake of tryptophan by brain.
STALOSYLGALACTOSYL CERAMTDE AS A SPECIFIC MARKER FOR HUMAN MYELIN AND OLIGODENDROGLIAL PERIKARYA: GANGLIOSIDES OF HUMAN MYELIN, OLIGODENDROGLIA AND NEURONS
Authors: Yu Robert K. , Iqbal Khalid 
Published: October 2006

Abstract—Gangliosides were isolated from human brain myelin, oligodendroglia, and neurons. Quantitative analysis revealed the following ganglioside contents: myelin, 2.0; neurons, 1.3; and oligodendroglia, 0.35 μg ganglioside sialic acid per mg protein. Myclin had a relatively simple ganglioside pattern with GM4and GM1as the predominant ganglioside species. The ganglioside pattern of oligodendroglia was quite complex and it resembled that of whole white matter rather than that of myelin. A high concentration of GM4was found in oligodendroglial fractions in addition to GM1, GD1a, GD1b, and GT1b. The usually‐ minor brain gangliosides GM3, GM2, and GM3were also enriched in oligodendroglia. The neuronal ganglioside pattern was generally similar to the pattern of whole gray matter. Both neurons and whole gray matter contained very low amounts of GM4. These results indicate that GM4is specifically localized in myelin and oligodendroglia of the CNS. Evidence is also presented that myelin, but not oligodendroglia, is the major reservoir of human white matter GM1and GM4.
ROLE OF ADENOSINE 3′, 5′‐MONOPHOSPHATE IN THE REGULATION OF CIRCADIAN OSCILLATION OF SEROTONIN N‐ACETYLTRANSFERASE ACTIVITY IN CULTURED CHICKEN PINEAL GLAND
Authors: Deguchi Takeo 
Published: October 2006

Abstract—When pineal glands of 10–12‐day‐old chicks were organ‐cultured in darkness, serotonin N‐acetyltransferase activity was low during the daytime, increased at midnight and then decreased to the daytime level the next morning. The pattern of increase and decrease of enzyme activity in cultured pineal glands was comparable to the circadian rhythm of N‐acetyltransferase activity in vivo. When pineal glands were kept at a low temperature for 5 h prior to culture, the phase of autonomous rhythm of enzyme activity was delayed. When chicken pineal glands were cultured during the daytime for 6 h, derivatives of adenosine 3′, 5′‐monophosphate (cyclic AMP), cholera toxin, a high concentration of KCl and phosphodiesterase inhibitors increased N‐acetyltransferase activity 3–7‐fold, indicating an involvement of cyclic AMP in the regulation of N‐acetyltransferase activity in chicken pineal gland as has been shown in rat pineal gland. When pineal glands were cultured at night in darkness, cholera toxin or a high KCl did not enhance the night‐time increase of the enzyme activity. Derivatives of cyclic AMP or phosphodiesterase inhibitors enhanced the autonomous night‐time increase of N‐acetyltransferase activity in an additive or more than additive manner in cultured pineal glands. These observations suggest that adenylate cyclase of pinealocytes is inactive during daytime, but is activated at night in darkness, which is transduced to the synthesis of N‐acetyltransferase molecules. Catecholamines suppressed the basal level and the nocturnal increase of N‐acetyltransferase activity via α‐adrenergic receptor. The nocturnal increase of enzyme activity was prevented by cycloheximide or actinomycin D. Cocaine, which stabilizes cell membrane potential or light exposure, blocked the nighttime increase of N‐acetyltransferase activity in cultured chicken pineal glands.
Taurine in Developing Rhesus Monkey Brain
Authors: Sturman J. A. , Rassin D. K. , Gaull G. E. , Cote L. J. 
Published: October 2006

AbstractThe concentrations of taurine in all regions of fetal and neonatal rhesus monkey brain are greater than in the same regions of adult monkey brain. [35S]Taurine injected into pregnant rhesus monkeys is accumulated by the fetus. This process occurs rapidly in most tissues, but occurs slowly in fetal brain. Neonatal rhesus monkey brain also accumulates [35S]taurine slowly compared with other tissues after i.v. injection, and continues to accumulate [35S]taurine for a long period of time. These results suggest that the accumulation and exchange of taurine in developing rhesus monkey brain is slow, as found in neonatal rats, and that if there is a period of development at which rapid exchange of brain taurine occurs in the rhesus monkey, it is before the rapid brain growth spurt.
Long‐chain Fatty Acid:CoA Ligase in Rat Brain in vitro: A Comparison of Activities with Oleic and cis‐Vaccenic Acids
Authors: Murphy M. G. , Spence M. W. 
Published: October 2006

Abstract:Long‐chain fatty acid:CoA ligase (EC 6.2.1.3) has been examined in vitro with brain preparations from 12‐ to 16‐day‐old rats using oleic (18: 1[n‐9]) and cis‐vaccenic (18: 1[n‐7]) acids. A novel assay system, which permits measurement of product as [14C]fatty acyl‐[3H]CoA, [14C]fatty acyl‐CoA, or fatty acyl‐[3H]CoA, was used. With the double‐label assay, reaction conditions were established that gave a molar ratio of [3H]CoA to [14C]fatty acid in the product of 1.06 ± 0.12 (mean ±s.d., n= 14). This indicates that the method is specific for the fatty acid added to the incubation mixture. The assay is sensitive to the formation of approximately 0.02 nmol fatty acyl‐CoA. With oleic acid, specific activity of the ligase was highest in a microsomal fraction (3.91 ± 0.55 nmol oleoyl‐CoA formed/min/mg protein; n= 16). Optimal activity was obtained at concentrations of fatty acid, CoA, ATP and Mg2+ of 50 μM, 50 μM, 10 mm, and 8 mm, respectively. The apparent Kms (approximate) for oleic acid and coenzyme A were 20 and 6 μM, respectively. With cis‐vaccenic acid (18:1[n‐7]), a naturally occurring isomer of oleate, the maximum reaction rate was higher than that with oleate, as were the apparent Kms for both fatty acid (105 μM) and coenzyme A (23 μM).
Effect of Thyrotropin‐Releasing Hormone (TRH) on Local Cerebral Glucose Utilization, by the Autoradiographic 2‐Deoxy[14C]glucose Method, in Conscious and Pentobarbitalized Rats
Authors: Nagai Y. , Narumi S. , Nagawa Y. , Sakuradat O. , Uenot H. , Ishii S. 
Published: October 2006

Abstract:Effects of TRH and pentobarbital alone, and in combination, on local cerebral glucose utilization of rats were studied by the autoradiographic 2‐deoxy[14C] glucose method. TRH (5 mg/kg i.v.) reduced the rate of cerebral glucose utilization slightly in the whole brain. Locally, significant depression was observed in the following structures: frontal and visual cortices, hippocampus Ammon's horn and dentate gyrus, medial and lateral geniculate bodies, nucleus accumbens, caudate‐putamen, substantia nigra, pontine gray matter, superior colliculus, superior olivary nucleus, vestibular nucleus, lateral lemniscus and cerebellar cortex. Pentobarbital (30 mg/kg i.v.) produced a marked and diffuse reduction in the rate of glucose utilization throughout the brain. TRH given 15 min after the administration of pentobarbital markedly shortened the pentobarbital sleeping time and caused some reversal of the depression in local cerebral glucose utilization produced by pentobarbital. These effects were almost completely abolished by pretreatment with intracerebroventricular injection of atropine methyl bromide (20 μg/rat). These results indicate that although TRH acts to cause a reduction in the rate of cerebral glucose utilization, it reverses the depression induced by pentobarbital, via a cholinergic mechanism, in a number of structures, some of which are related to monoaminergic systems and the reticulo‐thalamo‐cortical activating system. Nagai Y. et al. Effect of thyrotropin‐releasing hormone (TRH) on local cerebral glucose utilization, by the autoradiographic 2‐deoxy[14C]glucose method, in conscious and pentobarbitalized rats. J. Neurochem.35, 963‐971 (1980).
Changes in Muscarinic Binding in Distant Brain Regions Showing Neuronal Losses After Folic Acid Injections into the Substantia Innominata
Authors: Wong P. T.‐H. , McGeer E. G. , Singh K. , McGeer P. L. 
Published: October 2006

Abstract:Injection of folic acid (FA) into the nucleus substantia innominata (NSI) was found to decrease [3H]quinuclidinyl benzilate ([3H]QNB) binding in the frontal cortex, pyriform cortex, amygdala, and the NSI itself without changing the Kd. Binding in the thalamus, caudate nucleus, hippocampus, and substantia nigra was not affected. [3H]Flunitrazepam binding was unchanged in all eight regions studied. Previous work indicates FA injections into the NSI produce epileptiform activity and cause loss of GABAergic and possibly other neurons in the frontal and pyriform cortices, the amygdala, and thalamus. The reductions of [3H]QNB binding in the first three of these regions are interpreted as indicating that many of the neurons lost are cholinoceptive, a finding that supports the previous hypothesis that activation of cholinergic projections from the NSI is an important part of the mechanism of cell loss in these regions.
Effects of Insulin and Streptozotocin‐Induced Diabetes on Brain Norepinephrine Metabolism in Rats
Authors: Trulson M. E. , Himmel C. D. 
Published: October 2006

Abstract:Administration of insulin (2 IU/kg, i.p.) produced a significant decrease (18%) in forebrain norepinephrine and a significant increase in the major metabolite of norepinephrine, 3‐methoxy‐4‐hydroxyphenyl‐glycol‐sulfate (MOPEG‐SO4, +19%) in rats. Streptozotocin‐induced diabetes produced the opposite effects, resulting in an increase in forebrain norepinephrine (+17%) and a decrease in MOPEG‐SO4 (−26%). In addition, insulin increased (+143%) and diabetes decreased (− 41%) the turnover rate of norepinephrine, as measured by the rate of decrease of norepinephrine following inhibition of tyrosine hydroxylase by α‐methyl‐P‐tyrosine. All of these effects in diabetic rats were reversed by insulin replacement therapy. These data are discussed within the context of mood disorders characteristic of diabetic patients.
Intracellular pH and Catecholamine Synthesis in Cultured Bovine Adrenal Medullary Cells: Effect of Extracellular Na+ Removal
Authors: Yanagihara Nobuyuki , Yokota Kenji , Wada Akihiko , Izumi Futoshi 
Published: October 2006

Abstract:Incubation of cultured bovine adrenal medullary cells in Na+‐free sucrose medium or in Na+‐free Cs+ medium enhanced the synthesis of 14C‐catecholamines from [14C]tyrosine about two‐ to threefold or sixfold, respectively. The increment of 14C‐catecholamine synthesis produced by Na+‐free medium was partially dependent on the presence of Ca2+ in the medium. Dibutyrylcyclic AMP also stimulated the synthesis of 14C‐catecholamines in adrenal medullary cells, and the effects of Na+ removal and dibutyryl cyclic AMP (5 mM) on the synthesis were almost additive. The intracellular pH measured by using a weak acid 5, 5‐dimethyloxazolidine‐2, 4‐dione was 7.14 in control cells and when Na+ was replaced by sucrose or Cs+, it shifted down to 6.56 or 5.66, respectively. The fall in intracellular pH and the stimulation of 14C‐catecholamine synthesis were similarly dependent on the concentration of Na+ in the medium. The optimal pH of soluble tyrosine hydroxylase was 5.5–6.0 both in control cells and in cells incubated in Na+‐free med um. These results suggest that removal of extracellular Na+ increases the synthesis of catecholamines, at least in part, by shifting the intracellular pH toward the optimal pH of tyrosine hydroxylase.
Ammonia‐Induced Release of Neurotransmitters from Rat Brain Synaptosomes: Differences Between the Effects on Amines and Amino Acids
Authors: Erecinska Maria , Pastuszko Anna , Wilson David F. , Nelson David 
Published: October 2006

Abstract:The effect of NH4Cl on release of amine and amino acid transmitters from rat brain synaptosomes was investigated. Ammonia (0.1–10 mM) stimulated the secretion of dopamine and 5‐hydroxytryptamine in a dose‐dependent manner, in a process which was additive with the effect of 40 mM K+, almost unaffected by withdrawal of Ca2+, and markedly decreased by increasing [H+] in the medium. The NH4Cl‐induced dopamine efflux, in contrast to that caused by high [K+]e, was inhibited by benztropine. The release of γ‐aminobutyric acid, aspartate, and glutamate was unaltered by [NH4Cl] < 5 mM, but somewhat stimulated at higher levels. Transmembrane pH gradient, acid inside, was dissipated by NH4Cl in a concentration‐dependent manner and the internal alkalinization correlated with the stimulation of the rate of dopamine efflux. Transmembrane electrical potential was unaffected by [ammonia] < 5 mM, but a small depolarization was observed at higher levels. It is postulated that ammonia‐induced alkalinization of the intrasynaptic storage granules causes extrusion of amines into the cytoplasm and their subsequent leakage into the medium through a reversal of the plasma membrane transporters. A lack of correlation between the release of amino acid neurotransmitters and the dissipation of the ΔpH suggests that in rat brain intrasynaptic vesicles, acidic inside, are unlikely to store substantial amounts of γ‐aminobutyric acid, aspartate, or glutamate.
Metalloendoprotease Cleavage of 18.2‐ and 14.1‐Kilodalton Basic Proteins Dissociating from Rodent Myelin Membranes Generates 10.0‐ and 5.9‐Kilodalton G‐Terminal Fragments
Authors: Chantry Andrew , Earl Christopher , Groome Nigel , Glynn Paul 
Published: October 2006

AbstractRat and guinea pig myelin membranes were incubated at physiological ionic strength with millimolar concentrations of Ca2+/Mg2+ ions (37°C; pH 7.4). After 1‐3 h, electrophoresis of the membranes revealed loss of 50% of 18.2‐ and 14.1‐kilodalton (kDa) forms of myelin basic protein (MBP). Concomitantly, peptides representing 25% of the original membrane‐associated MBP were detected in incubation media. Roughly equal amounts of MBP fragments with molecular masses of 10.0 and 8.4 kDa were found in media from guinea pig myelin incubations. Media from rat myelin experiments contained a major 8.4‐kDa and minor 10.0‐ and 5.9‐kDa MBP peptides. Kinetic studies implied that proteolysis occurred subsequent to MBP dissociation from the membranes. Immunoblotting studies indicated that both the 18.2‐and 14.1‐kDa forms of MBP were cleaved near residue 73 to produce a 10.0‐ and 5.9‐kDa C‐terminal fragment, respectively. Degradation of MBP in myelin membranes was partially inhibited by only 5‐20% using leupeptin (20 μM), N‐ethylmaleimide (10 mM), phenylmethylsulphonyl fluoride (1 mM), and phos‐phoramidon (50 μM) but up to 50% by dithiothreitol (DTT, 10 mM). Only DTT and 1,10‐phenanthroline substantially blocked the formation of the characteristic 10.0‐and 5.9‐kDa C‐terminal fragments. This suggests that MBP, dissociating from myelin membrane preparations, is cleaved near residue 73 by a metalloendoprotease distinct from N‐ethylmaleimide/leupeptin‐sensitive calpains and phosphoramidon‐sensitive endopeptidase 24.11.
Cyclic Nucleotides and the Activity of Glia Maturation Factor in the Hypoplastic Cerebellum of Developing Jaundiced Gunn Rats
Authors: Aono Sachiko , Kato Taiji , Tanaka Ryo , Sato Hiroshi , Semba Reiji , Kashiwamata Shigeo 
Published: October 2006

AbstractDevelopmental changes of cyclic nucleotides were studied in the hypoplastic cerebellum of jaundiced Gunn rats over the period of postnatal days 8 to 30. The mitogenic activity of glia maturation factor was also measured at day 15. In jaundiced homozygotes(jj), the amount of cyclic GMP on a protein basis was not significantly different from that in control heterozygotes (j+) at either day 8 or 15, but at day 30 it was reduced to about 19% of the control. On the other hand, a lowered nucleotide level on a wet weight basis in jj rats was already statistically significant at day 15. In contrast to cyclic GMP, the rates of increase of cyclic AMP on a wet weight basis were almost the same in the two groups of rats, but the nucleotide levels on a protein basis at days 15 and 30 were a little, but significantly, higher in jj rats than in j+ rats. The activity of glia maturation factor in jj rats was found to be 1.5‐3 times as high as that in j+ rats. Possible implications of the present results are discussed.
Octopamine Uptake and Metabolism in the Insect Nervous System
Authors: Wierenga Joel M. , Hollingworth Robert M. 
Published: October 2006

Abstract:Several insect tissues were examined for their ability to take up octopamine in the presence and absence of sodium ions. The cockroach Malpighian tubules, ovary, and ventral nerve cord showed the highest level of sodium‐dependent uptake. The adult firefly lantern exhibited substantial sodiumindependent uptake. Some of these tissues were also examined for their ability to metabolize octopamine by N‐acetylation. Measurable N‐acetyltransferase activity was present in the cockroach ventral nerve cord, tobacco hornworm CNS, and firefly light organ. N‐Acetylation is proposed to be the major metabolic pathway for octopamine in the cockroach (Periplaneta americana) nervous system. Several classes of compounds, including octopamine receptor agonists, tricyclic antidepressants, amphetamines, chloroethylbenzylamines, and some experimental insecticides, were tested for their ability to inhibit octopamine uptake and metabolism. The sodium‐insensitive component of uptake was not inhibited by most compounds tested, but the sodium‐sensitive component was strongly inhibited by xylamine, N‐ethyl‐N‐chloroethyl‐o‐bromobenzylamine, and their aziridinium ions (60–100%). These compounds also effectively inhibited N‐acetyltransferase (IC50 values at or below 1 μM). Other good inhibitors of N‐acetyltransferase included desipramine, synephrine, and an experimental insecticide, CGA 132427. Formamidine pesticides had limited effect on both processes, and neither action seems likely to be involved in their octopaminergic actions in vivo. Cocaine was unique in stimulating N‐acetyltransferase activity. When inhibition of sodium‐sensitive uptake is compared with inhibition of N‐acetyltransferase in the cockroach ventral nerve cord, two groups of inhibitors are discernible. Type 1 compounds inhibit uptake without an effect on N‐acetyltransferase, whereas type 2 compounds inhibit both processes. These results suggest a functional linkage between the uptake and acetylation of octopamine.
Acid Lability of Metabolites of 2‐Deoxyglucose in Rat Brain: Implications for Estimates of Kinetic Parameters of Deoxyglucose Phosphorylation and Transport Between Blood and Brain
Authors: Dienel Gerald A. , Cruz Nancy F. , Mori Kentaro , Sokoloff Louis 
Published: October 2006

Abstract:The steady‐state brain/plasma distribution ratios of [14C]deoxyglucose ([14C]DG) for hypoglycemic rats previously determined by measurement of DG concentrations in neutralized acid extracts of freeze‐blown brain and plasma exceeded those predicted by simulations of kinetics of the DG model. Overestimation of the true size of the precursor pool of [14C]DG for transport and phosphorylation could arise from sequestration of [14C]DG within brain compartments and/or instability of metabolites of [14C] DG and regeneration of free [14C]DG during the experimental period or extraction procedure. In the present study, the concentrations of [14C]DG and glucose were compared in samples of rat brain and plasma extracted in parallel with perchloric acid or 65% ethanol containing phosphate‐buffered saline. The concentrations of both hexoses in acid extracts of brain were higher than those in ethanol, whereas hexose contents of plasma were not dependent on the extraction procedure. The magnitude of overestimation of DG content (about 1.2 to fourfold) varied with glucose level and was highest in extracts isolated from hypoglycemic rats; contamination of the [14C]DG fraction with 14C‐labeled nonacidic metabolites also contributed to this overestimation. Glucose concentrations in acid extracts of brain exceeded those of the ethanol extracts by < 40% for normal and hypoglycemic rats.
Prevention of hepatic fibrosis in nonobese diabetic mice: a critical role for interferon‐γ
Authors: Mukai Tsuyoshi , Nagaki Masahito , Imose Motoaki , Kimura Kiminori , Satake Shinichi , Takai Shinji , Moriwaki Hisataka 
Published: September 2006

Abstract: Background/Aims: Nonobese diabetic (NOD) mice, a model of type I diabetes mellitus, harbor certain unique defects in their immune system. The aim of this study was to investigate how NOD mice show hepatic injury and subsequent fibrogenic responses.Methods: Hepatic fibrosis was induced by intraperitoneal injections of dimethylnitrosamine (DMN), and assessed biochemically and histologically. Expressions of cytokine messenger RNA (mRNA) in the liver were determined.Results: In a model of liver cirrhosis induced by dimethylnitrosamine (DMN), we found that NOD mice had lower levels of hepatic fibrosis and better survival than control ICR mice. The resistance to DMN‐induced lethality in NOD mice was independent of apoptosis and necrosis of hepatocytes, but apparently due to the prevention of hepatic fibrosis. We also found increased inductions of interferon‐γ (IFN‐γ) mRNA in the liver of NOD mice and of intracellular IFN‐γ from intrahepatic T cells following DMN administration. Treatment with neutralizing anti‐IFN‐γ‐antibody cancelled the inhibition of hepatic fibrosis in NOD mice.Conclusions: These results suggest that IFN‐γ is effective for inhibiting hepatic fibrosis and that genetic host factors may be important in determining differential responses to injury.