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  • 1
    Keywords: Oxygen--Physiological transport--Congresses. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (394 pages)
    Edition: 1st ed.
    ISBN: 9781461502050
    Series Statement: Advances in Experimental Medicine and Biology Series ; v.510
    Language: English
    Note: OXYGEN TRANSPORT TO TISSUE XXIII -- Editor's page -- Copyright -- INTERNATIONAL SOCIETY ON OXYGEN TRANSPORT TO TISSUE 2001 -- SPONSORS -- PREFACE -- CONTENTS -- THE ROLE OF TUMOR OXYGENATION IN VASCULAR AND CLINICAL RESPONSE TO ANGIOGENESIS INHIBITION -- COMPARISON OF FLUCTUATIONS OF OXYGEN TENSION IN FSA, 9L, AND R3230AC TUMORS IN RATS -- EFFECT OF CARBOGEN-BREATHING ON REDOX STATUS OF THE RIF-1 TUMOR -- EVALUATION OF MICROREGIONAL VARIATIONS IN TUMOR HYPOXIA FOLLOWING THE ADMINISTRATION OF ENDOSTATIN -- EFFECT OF HYDRALAZINE ON BLOOD FLOW, OXYGENATION, AND INTERSTITIAL FLUID PRESSURE IN SUBCUTANEOUS TUMORS -- OXYGENATION OF CERVIX CANCERS: IMPACT OF CLINICAL AND PATHOLOGICAL PARAMETERS -- QUANTITATIVE SPATIAL ANALYSIS OF HYPOXIA AND VASCULAR PERFUSION IN TUMOR SECTIONS* -- TUMOR OXYGENATION AND ITS RELEVANCE TO TUMOR PHYSIOLOGY AND TREATMENT -- MECHANISMS UNDERLYING HYPOXIA DEVELOPMENT IN TUMORS -- LACK OF ASSOCIATION BETWEEN TUMOR HYPOXIA, GLUT-1 EXPRESSION AND GLUCOSE UPTAKE IN EXPERIMENTAL SARCOMAS -- THE IMPACT OF TISSUE MICROENVIRONMENT ON TREATMENT SIMULATION -- EVIDENCE FOR AND AGAINST HYPOXIA AS THE PRIMARY CAUSE OF TUMOR AGGRESSIVENESS -- CHARACTERIZATION OF HUMAN Gc PROTEIN-DERIVED MACROPHAGE ACTIVATION FACTOR (GcMAF) AND ITS FUNCTIONAL ROLE IN MACROPHAGE TUMORICIDAL ACTIVITY -- EFFECT OF HEMOGLOBIN SOLUTIONS AS HEMODILUENTS ON CAPILLARY OXYGEN TENSION -- DIFFERENT EFFICACY IN VITRO OF HEMOGLOBIN BASED OXYGEN CARRIERS AND RED CELLS -- A NOVEL BLOOD TRANSFUSANT CANDIDATE: INTACT HUMAN ERYTHROCYTES CONTAINING HEMOGLOBIN EXCLUSIVELY NITROSYLATED IN THE α-SUBUNITS -- THE CONTRIBUTION OF HEMOGLOBIN TO OXYGEN TRANSPORT IN THE MICROCRUSTACEAN DAPHNIA MAGNA -- MODIFICATIONS OF RED BLOOD CELL SHAPE AND GLYCOPROTEINS MEMBRANE CONTENT IN SEPTIC PATIENTS. , FIBER OPTIC IMMUNOSENSORS FOR CARDIOVASCULAR DISEASE DIAGNOSIS: Quantification of Protein C, Factor V Leiden, and cardiac Troponin T in plasma -- SOFT GEL CHROMATOGRAPHY COLUMN ANALYSIS AND DESIGN FOR THE PRODUCTION OF HIGH MOLECULAR WEIGHT BLOOD FACTORS: MODEL MOLECULE PROTEIN C -- DEVELOPMENT OF AN ECONOMIC MINIANTIBODY PRODUCTION PROCESS FOR THE PURIFICATION OF PROTEIN C (ANTI-COAGULANT/ANTI-THROMBOTIC) -- NITRIC OXIDE SYNTHESIS IN BRAIN IS STIMULATED BY OXYGEN -- OXYGEN INDIRECTLY REGULATES NITRIC OXIDE AVAILABILITY -- MODELING THE REGULATION OF OXYGEN CONSUMPTION BY NITRIC OXIDE -- OXYGEN SENSOR DESIGN: ANALYSIS AND CORRECTION OF PROBLEMS ASSOCIATED WITH ZERO CURRENT, STABILITY AND STRUCTURE -- COMPUTER SIMULATION OF OXYGEN MICROELECTRODE MEASUREMENTS IN TISSUES -- PHYSIOLOGICAL OXYGEN MEASUREMENTS USING OXYGEN ELECTRODES -- ACCURACY OF A POLAROGRAPHIC ELECTRODE AT HIGH OXYGEN CONCENTRATIONS -- RECESSED OXYGEN ELECTRODES: GETTING MORE THAN PO2 -- OXYGEN DISTRIBUTIONS IN TISSUE MEASURED BY PHOSPHORESCENCE QUENCHING -- ADAPTING AND VALIDATING A NIRS DEVICE TO MEASURE IN UTERO FETAL SHEEP CEREBRAL OXYGENATION -- DETECTION OF THE FAST NEURONAL SIGNAL ON THE MOTOR CORTEX USING FUNCTIONAL FREQUENCY DOMAIN NEAR INFRARED SPECTROSCOPY -- Probing Rat Brain Oxygenation with Near-Infrared Spectroscopy (NIRS) and Magnetic Resonance Imaging (MRI) -- VARIATION IN BLOOD OXYGENATION AND CEREBRAL pO2 IN A MOUSE MODEL MEASURED BY EPR SPECTROMETRY -- FUNCTIONAL OXYGEN-17 MAGNETIC RESONANCE IMAGING AND LOCALIZED SPECTROSCOPY -- DEVELOPMENT OF A RETRACTOR FOR MONITORING THE OXYGENATION STATE OF BRAIN TISSUE -- MAPPING OF HEMODYNAMICS ON THE HUMAN CALF WITH NEAR INFRARED SPECTROSCOPY AND THE INFLUENCE OF THE ADIPOSE TISSUE THICKNESS -- EPR IMAGING OF VASCULAR CHANGES IN OXYGEN IN RESPONSE TO CARBOGEN BREATHING -- MOLECULAR IMAGING BY PET. , FREQUENCY DOMAIN IMAGING OF OXYGEN TENSION IN THE MOUSE RETINA -- OXYGEN DELIVERY TO THE RETINA AND RELATED VISUAL PATHOLOGY -- ACTIVATION OF THE VISUAL CORTEX IN NEWBORN INFANTS UNDER NATURAL SLEEP USING MULTICHANNEL NEAR-INFRARED SPECTROSCOPY -- EFFECT OF BLOOD FLOW ON PvO2-VO2 RELATION IN CONTRACTING IN SITU SKELETAL MUSCLE -- OXYGEN TRANSPORT AND INTRACELLULAR BIOENERGETICS ON STIMULATED CAT SKELETAL MUSCLE -- MUSCLE OXYGENATION BY NEAR INFRARED SPECTROSCOPY AND LACTATE THRESHOLDS IN ENDURANCE TRAINED AND RECREATIONALLY ACTIVE CYCLISTS -- CARDIAC OUTPUT, OXYGEN CONSUMPTION AND MUSCLE OXYGEN DELIVERY IN SUBMAXIMAL EXERCISE -- NON-INVASIVE PET AND SPECT IMAGING OF TISSUE HYPOXIA USING ISOTOPICALLY LABELED 2-NITROIMIDAZOLES+ -- DIFFUSE OPTICAL MEASUREMENT OF HEMOGLOBIN AND CEREBRAL BLOOD FLOW IN RAT BRAIN DURING HYPERCAPNIA, HYPOXIA AND CARDIAC ARREST -- MULTIORGAN MONITORING OF HEMODYNAMIC AND MITOCHONDRIAL RESPONSES TO ANOXIA AND CARDIAC ARREST IN THE RAT -- IMPORTANCE OF GLOMUS CELL PLASMA MEMBRANE AND MITOCHONDRIAL MEMBRANE POTENTIALS DURING ACUTE HYPOXIA SIGNALING IN THE RAT CAROTID BODY -- ESTIMATION OF HYDROXYL RADICALS BASED ON THE SALICYLATE TRAPPING METHOD IN HIPPOCAMPUS OF STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS (SHRSP) DURING TRANSIENT ISCHEMIA AND RECIRCULATION -- EFFECT OF HYPOXIA AND ISCHEMIA ON EXPRESSION OF SELECTED GENES IN BRAIN OF NEWBORN PIGLETS -- BRAIN OXYGENATION DURING CARDIOPULMONARY BYPASS AND CIRCULATORY ARREST -- EXPRESSION OF ANGIOPOIETIN-1 AND -2 IN THE RAT BRAIN DURING CHRONIC HYPOXIA AND DE-ADAPTATION -- HYPOXIA-INDUCIBLE FACTOR-1α ACCUMULATION IN THE RAT BRAIN IN RESPONSE TO HYPOXIA AND ISCHEMIA IS ATTENUATED DURING AGING -- LUNG ISCHEMIA: ENDOTHELIAL CELL SIGNALING BY REACTIVE OXYGEN SPECIES -- NEAR INFRARED SPECTROSCOPY (NIRS) MEASUREMENTS DURING GLOBAL CEREBRAL ISCHEMIA IN SHEEP. , SIMULATIONS OF CAPILLARY NETWORK OXYGEN TRANSPORT DURING TRANSIENT ISCHEMIA IN THE PRESENCE AND ABSENCE OF TISSUE MYOGLOBIN -- CEREBRAL OXYGENATION DURING CHRONIC OBSTRUCTIVE PULMONARY DISEASE+ -- PHYSIOLOGY OF FUNCTIONAL ACTIVATION -- NONLINEAR ANALYSIS OF HEART RATE VARIABILITY IN INFANTS WITH APPARENT LIFE-THREATENING EVENTS -- THE EFFECT OF NICOTINAMIDE & -- HYPEROXIC GASES ON BLOOD GLUCOSE -- MEASUREMENT OF TISSUE OXYGENATION INDEX DURING THE FIRST THREE DAYS IN PREMATURE BORN INFANTS -- SIMULTANEOUS MEASUREMENT OF CEREBRAL TISSUE OXYGENATION OVER THE ADULT FRONTAL AND MOTOR CORTEX DURING REST AND FUNCTIONAL ACTIVATION -- DYSFUNCTIONAL MICROVASCULAR CONDUCTED RESPONSE IN IRRADIATED NORMAL TISSUE -- OXYGENATION AND BLOOD CONCENTRATION CHANGES IN HUMAN SUBJECT PREFRONTAL ACTIVATION BY ANAGRAM SOLUTIONS -- QUANTITATION OF THE CONCORDANCE BETWEEN CEREBRAL INTRAVASCULAR OXYGENATION AND MEAN ARTERIAL BLOOD PRESSURE FOR THE DETECTION OF IMPAIRED AUTOREGULATION -- EFFECTS OF FLUID PERCUSSION INJURY ON RAT BRAIN HEMODYNAMICS, IONIC, ELECTRICAL ACTIVITY, AND ENERGY METABOLISM IN VIVO -- AUTHOR INDEX -- SUBJECT INDEX.
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 46 (1986), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Rat brain synaptosomes exhibit calcium-dependent transglutaminase activity. This activity, measured in detergent-treated or sonicated preparations, was six- to sevenfold lower than that in the liver. The synaptosomal transglutaminase was inhibited by various amines and α-difluoromethylornithine, compounds known to inhibit activity of this enzyme in other tissues. The inhibitors of transglutaminase induced release of catecholamines, but not of γ-aminobutyric acid, from synaptosomes both under basal and K+-stimulated conditions. The concentrations of the agents that caused stimulation of catecholamine release were approximately the same as those that inhibited the activity of transglutaminase. Stimulation of release was largely reduced by the withdrawal of calcium from the incubation medium. Inhibitors of transglutaminase had little effect either on the uptakes of neurotransmitters or the amounts of deaminated products of catecholamine degradation released into the medium. It is suggested that a synaptosomal transglutaminase is involved in suppressing vesicular release of catecholamines by resting (nondepolarized) neurons and that this action may also be a part of negative feedback control which prevents excessive transmitter release at the synapse during increased neuronal activity.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The present study describes the relationships of extracellular striatal dopamine, cortical oxygen pressure, and striatal hydroxyl radicals in brain of newborn piglets during hypoxia and posthypoxic reoxygenation. Hypoxia was induced by reducing the fraction of inspired oxygen (FiO2) from 22% (control) to 7% for 1 h. The FiO2 was then returned to the control value and measurements were continued for 2 h. Cerebral oxygen pressure was measured by the oxygen dependent quenching of phosphorescence and extracellular levels of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and hydroxy radicals in the striatum were determined by in vivo microdialysis. Hypoxia decreased the cortical oxygen pressure from 47 ± 2 to 9 ± 1.3 torr (p 〈 0.001); the levels of extracellular dopamine in the striatum increased to 16,000 ± 3,270% of control (p 〈 0.01), whereas the levels of DOPAC and HVA decreased to 25.3 ± 6% (p 〈 0.001) and 36 ± 5% (p 〈 0.01) of control, respectively. Compared with control, the hydroxyl radical levels at each time point were not significantly increased during hypoxia, although the sum of the measured values was significantly increased (p 〈 0.05). During the first 5 min after FiO2 was returned to 22%, the cortical oxygen pressure increased to control values and stayed at this level for the remainder of the measurement period. The extracellular level of dopamine declined to values not statistically different from control during 40 min of reoxygenation. During the first 10 min of reoxygenation, DOPAC and HVA further decreased and then began to slowly increase. By 70 min of reoxygenation, the values were not significantly different from control. Hydroxyl radicals were above control during the entire period of reoxygenation, with maximal values observed after 100 min of reoxygenation. This increase was largely abolished by injecting the animals with α-methyl-p-tyrosine 5 h before hypoxia, a procedure that depleted the brain of dopamine. Our results suggest that oxidation of striatal dopamine during posthypoxic reoxygenation is at least partly responsible for the observed increase in striatal level of hydroxyl radicals that may exacerbate posthypoxic cerebral injury.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The present study tests the hypothesis that ventilation with 100% O2 during recovery from asphyxia leads to greater disturbance in brain function, as measured by dopamine metabolism, than does ventilation with 21% oxygen. This hypothesis was tested using mechanically ventilated, anesthetized newborn piglets as an animal model. Cortical oxygen pressure was measured by the oxygen-dependent quenching of phosphorescence, striatal blood flow by laser Doppler, and the extracellular levels of dopamine and its metabolites by in vivo microdialysis. After establishment of a baseline, both the fraction of inspired oxygen (FiO2) and the ventilator rate were reduced in a stepwise fashion every 20 min over a 1-h period. For the subsequent 2-h recovery, the animals were randomized to breathing 21 or 100% oxygen. It was observed that during asphyxia cortical oxygen pressure decreased from 36 to 7 torr, extracellular dopamine increased 8,300%, and dihydroxyphenylacetic acid and homovanillic acid decreased by 65 and 60%, respectively, compared with controls. During reoxygenation after asphyxia, cortical oxygen pressure was significantly higher in the piglets ventilated with 100% oxygen than in those ventilated with 21% oxygen (19 vs. 11 torr). During the first hour of reoxygenation, extracellular dopamine levels decreased to ∼200% of control in the 21% oxygen group, whereas these levels were still much higher in the 100% oxygen group (∼500% of control). After ∼2 h of reoxygenation, there was a secondary increase in extracellular dopamine to ∼750 and ∼3,000% of baseline for the animals ventilated with 21 and 100%, respectively. It is concluded that although 100% FiO2 after asphyxia increases cortical oxygenation compared with 21% FiO2, it also results in poorer recovery in dopamine metabolism and higher secondary release of striatal dopamine. The resulting increased extracellular levels of dopamine may exacerbate posthypoxic cerebral injury.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 60 (1993), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Neurocatin, a neuroregulatory factor isolated from mammalian brain, is a powerful affector of protein phosphorylation in rat striatal synaptosomes. Two major synaptosomal phosphoproteins of ∼80 and ∼60 kDa, possibly synapsin I and tyrosine hydroxylase, were especially sensitive to neurocatin. Immunoprecipitation experiments confirmed that the 60-kDa protein is the enzyme tyrosine hydroxylase. At low concentrations of neurocatin (to ∼7.5 ng/100 μl of suspension), incorporation of 32P orthophosphate into these proteins increased with increasing neurocatin concentration. At 7.5 ng of neurocatin, incorporation of the label into the two proteins increased by 22 and 26%, respectively. Concentrations of neurocatin 〉7.5 ng/100 μl caused progressive decrease in incorporation of 32P into many synaptosomal proteins; by a concentration of neurocatin of ∼45 ng/100 μ/l, the level of 32P incorporation into many proteins was ≤70% of control. The effects of neurocatin on synaptosomal protein phosphorylation were also dependent on the time of incubation. At a constant concentration of ∼7.5 ng/100 μl of neurocatin, increased incorporation of 32P into many proteins was measurable within 0.5 min and was maximal by 1 min. Incubation times 〉2.0 min, showed progressive decrease in 32P incorporation. Removing extrasynaptosomal Ca2+ with EGTA attenuated the increased 32P incorporation induced by low neurocatin concentrations, suggesting that calcium plays a role in neurocatin-induced phosphorylation of rat striatal synaptosomal proteins. The reduced incorporation of label induced by high neurocatin concentrations, however, was not calcium dependent. The effects of neurocatin on the level of 32P incorporation into proteins were observed only in intact synaptosomes, consistent with this compound acting through receptors on the plasma membrane.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of graded levels of tissue hypoxia on the extracellular levels of dopamine, 3,4-dihydroxyphenylacetic acid, homovanillic acid, and 5-hydroxyindoleacetic acid has been monitored in vivo by microdialysis. Reproducible levels of decreased oxygen in the brain were obtained by increasing the rate of ventilation from the control value of 25/min to as high as 95/min. With increasing ventilatory rate, the oxygen pressure in the cortex decreased from ∼40 torr to 16 torr. As the oxygen pressure decreased stepwise from 40 to 27, 22, and 16 torr, the dopamine levels in the extracellular medium rose by 70, 90, and 150%, respectively, returning to baseline within a few minutes of return to control ventilation rates. Levels of the catabolic products 3,4-dihydroxyphenylacetic acid, homovanillic acid, and 5-hydroxyindoleacetic acid decreased with decreasing tissue oxygen. Unlike the dopamine levels, these catabolite levels continued to decrease through 30 min of recovery (to 50% of control), returning to baseline only after recovery periods of 1–2 h. These data suggest that hypoxia induces long-term alterations in the neurotransmitter turnover. The marked effects of mild tissue hypoxia (decrease of oxygen from 40 torr to 26 torr) on both the extracellular dopamine concentration and dopamine metabolism indicate that the metabolic consequences of decreased tissue oxygen pressure extend to higher values than generally appreciated.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of graded hypoxia induced by hyperventilation on the activity of tyrosine hydroxylase was measured in vivo by microdialysis. Microdialysis probes were inserted into the striatum of newborn piglets and perfused with medium containing 3-hydroxybenzylhydrazine, an inhibitor of L-aromatic amino acid decarboxylase. The level of 3,4-dihydroxyphenylalanine (DOPA) measured in the effluent dialysate was then an index of tyrosine hydroxylase activity. The oxygen pressure in the veins and capillaries of the cortex was measured, through a cranial window placed over the parietal cortex, by the phosphorescence lifetime of palladium-meso-tetra(4-carboxyphenyl)porphine added to the blood. After baseline measurements, PaCO2 was decreased from 38 torr (control value) to 19, 13, and 11 torr resulting in decreases in the cortical oxygen pressure from 40 ± 6 torr to 26 ± 3, 23 ± 4, and 20 ± 4 torr, respectively. Decrease in the oxygen pressure to 26 ± 3 torr caused a statistically significant increase of 25–30% in the level of DOPA in the effluent perfusate. During the next step of increase in ventilator rate, when oxygen decreased only slightly, the level of DOPA remained at the higher level. Ventilation rates that lowered the oxygen pressure to below 20 torr, however, caused a progressive decrease in the level of DOPA. During recovery, the level of DOPA steadily increased, attaining 160% of control value after 1.5 h. When the oxygen pressure was decreased to 16 ± 2 torr by a single increase in ventilator rate, the DOPA level decreased in the effluent to 15–20% below control. With return of the ventilator rate to control values, the DOPA levels again increased to well above control and stayed higher even after 1.5 h. The slow return of tyrosine hydroxylase activity to control indicates relatively long-term modification of the enzyme activity. Activation of tyrosine hydroxylase occurs when the oxygen pressure is decreased, but at 〈16 torr the reaction rate becomes limited by the availability of oxygen and decreases with further decrease in oxygen pressure. Our results showed that even small changes in cortical oxygen pressure modulate the activity of tyrosine hydroxylase. This alteration in the metabolism of catecholamines in newborn brain may have significant impact on later development of the organism.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Incubation of synaptosomes from rat brain with dl-2-amino-5-phosphonovalerate (APV) stimulated an increased release of dopamine, and this effect was strictly dependent on the extrasynaptosomal calcium level. APV increased biosynthesis of dopamine from tyrosine by 30%, whereas monoamine oxidase activity was inhibited by 30%. When synaptosomes were incubated with radioactive dopamine, APV caused a large decrease in incorporation of label into 3,4-dihydroxyphenylacetic acid but greatly increased incorporation into norepinephrine and its N-methyl derivatives. Quantification of dopamine and its metabolites in synaptosomes, using electrochemical detection, indicated that the presence of APV resulted in changes in the absolute levels of the aforementioned dopamine metabolites similar to the changes in radiolabel incorporation. Omission of Ca2+ from the extrasynaptosomal medium greatly diminished the APV-induced changes in catecholamine metabolism. The metabolic changes appear to largely result from an increased intrasynaptosomal Ca2+ level due to the APV-induced increase in calcium permeability of the plasma membrane.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 47 (1986), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract Synaptosomes isolated from rat brain accumulated cysteic acid by a high-affinity transport system (Km= 12.3 ±2.1 μM; Vmax= 2.5 nmol mgprotein-1 min-1). This uptake was competitively inhibited by aspartate (Ki= 13.3 ± 1.8 μM) and cysteine sulfinate (Ki= 13.3 ± 2.3 μM). Addition of extrasynaptosomal cysteate, aspartate, or cysteine sulfinate to synaptosomes loaded with [35S]cysteate induced rapid efflux of the cysteate. This efflux occurred via stoichiometric exchange of amino acids with half-maximal rates at 5.0 ± 1.1 μM aspartate or 8.0 ± 1.3 μM a cysteine sulfinate. Conversely, added extrasynaptosomal cysteate exchanged for endogenous aspartate and glutamate with half-maximal rates at 5.0 ± 0.4 μM acysteate. In the steady state after maximal accumulation of cysteate, the intrasynaptosomal cysteate concentrations exceeded the extrasynaptosomal concentrations by up to 10,000-fold. The measured concentration ratios were the same, within experimental error, as those for aspartate and glutamate. Depolarization, with either high [K+] or veratridine, of the plasma membranes of synaptosomes loaded with cysteate caused parallel release of cysteate, aspartate, and glutamate. It is concluded that neurons transport cysteate, cysteine sulfinate, aspartate, and glutamate with the same transport system. This transport system catalyzes homoexchange and heteroex-change as well as net uptake and release of all these amino acids.
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  • 10
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 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.
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