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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Physica A: Statistical Mechanics and its Applications 172 (1991), S. 302-308 
    ISSN: 0378-4371
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Physics Letters A 182 (1993), S. 135-139 
    ISSN: 0375-9601
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 340 (1989), S. 52-61 
    ISSN: 1432-1912
    Keywords: Rabbit brain cortex ; Rat brain cortex ; Serotonin release ; Presynaptic serotonin autoreceptors ; Presynaptic α2-adrenoceptors ; Phentolamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Possible antagonist effects of phentolamine at presynaptic serotonin autoreceptors were studied in slices of the occipito-parietal cortices of the rabbit and the rat. The slices were preincubated with 3H-serotonin and then superfused and stimulated electrically with single pulses or pulse trains. Nitroquipazine 1 μmol/l, a compound that inhibits the high affinity neuronal uptake of serotonin, was present in the superfusion medium in all one pulse-experiments as well as in experiments in which the effect of unlabelled serotonin was examined. In rabbit cortical slices, unlabelled serotonin reduced the single pulse-evoked overflow of tritium. Its concentrationresponse curve was not changed by the selective α2-adrenoceptor antagonist idazoxan 1 μmol/l but was shifted to the right by phentolamine 1 and 10 μmol/l. Phentolamine 10 μmol/l also shifted to the right the concentration-inhibition curve of the selective 5-HT1-receptor agonist 5-carboxamidotryptamine. When the slices were stimulated by trains of 30 pulses at 3 Hz, phentolamine 1 and 10 μmol/l but not 0.1 μmol/l increased the evoked overflow of tritium, the maximal increase amounting to 178%; its effect was enhanced in the presence of nitroquipazine 1 μmol/l plus idazoxan 10 μmol/l (a drug combination that, when given alone, slightly increased the evoked overflow of tritium). The serotonin receptor antagonist metitepin at concentrations of 0.01–1 μmol/l also increased the overflow of tritium elicited by 30 pulses/3 Hz, the maximal increase amounting to 280%; its effect was potentiated in the presence of nitroquipazine 1 μmol/l plus idazoxan 10 μmol/l but was abolished or almost abolished in the presence of nitroquipazine 1 μmol/l plus phentolamine 10 μmol/l (a drug combination that, given alone, greatly increased the evoked overflow of tritium). When slices were stimulated by trains of 360 pulses at 3 Hz, there was no apparent antagonism of phentolamine 10 μmol/l against the inhibitory effect of unlabelled serotonin. In rat brain cortex slices, unlabelled serotonin reduced the overflow of tritium elicited by 4 pulses delivered at 100 Hz. Again, phentolamine 10 μmol/l shifted the concentration-response curve to the right. It is concluded that phentolamine blocks presynaptic serotonin autoreceptors in rabbit and rat brain cortex with pA2 values of 6.44 and 5.95, respectively. Previous failures to detect the antagonistic effect against exogenous agonists were probably due to stimulation conditions that led to marked endogenous autoinhibition of serotonin release. At least the major part of the increase by phentolamine of the release of serotonin is due to autoreceptor blockade rather than blockade of the presynaptic a2-adrenoceptors at the cortical serotoninergic axons.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 338 (1988), S. 250-255 
    ISSN: 1432-1912
    Keywords: Rat nucleus accumbens ; Rat nucleus caudatusputamen ; Acetylcholine release ; Dopamine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experiments in slices of rat nucleus accumbens were carried out in order to investigate whether the release of acetylcholine in this tissue is modulated through dopamine receptors. The slices were preincubated with 3H-choline and then superfused and stimulated electrically twice for 2 min each at a frequency of 3 Hz. The electrically evoked overflow of tritium averaged 2.9–3.9% of the tritium content of the tissue in the various groups. The D2-selective agonist quinpirole (0.01–1 μmol/l) reduced the evoked overflow of tritium by maximally 56%, an effect antagonized by the D2-selective antagonist (−)-sulpiride (1 μmol/l). The D1-selective agonist 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine (SKF 38393) caused a slight decrease only at the high concentration of 10 μmol/l. (−)-Sulpiride (0.1–10 μmol/l) moderately increased the evoked overflow of tritium when given alone. The dopamine uptake inhibitor nomifensine (10 μmol/l) caused a decrease, and in its presence the increase produced by (−)-sulpiride became much more marked, amounting to maximally 149%. (+)-Sulpiride (0.1–1 μmol/l) failed to change the evoked overflow of tritium in the presence of nomifensine. The dopamine-releasing agent (±)-amphetamine (1 μmol/l) also reduced the evoked overflow, an effect abolished by (−)-sulpiride. Finally, bretylium (1 mmol/l), which blocks the release of dopamine, increased the evoked overflow. (−)-Sulpiride (1 μmol/l) lost its facilitatory effect in slices treated with bretylium. We conclude that the release of acetylcholine in rat nucleus accumbens, like its release in the nucleus caudatusputamen, is modulated through dopamine D2-receptors. The receptors are activated by endogenous dopamine under the conditions of these experiments.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1106
    Keywords: Key words Substantia nigra ; MPTP ; Parkinsonism ; Primate ; Electrophysiology ; Basal ganglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The basal ganglia are currently viewed as components of segregated corticosubcortical reentrant circuits. One of these circuits, the ”motor” circuit, is critically involved in the development of parkinsonian motor signs. Current pathophysiologic models postulate that parkinsonism is associated with increased activity in the basal ganglia output nuclei. The neuronal activity in the motor portion of one of these output nuclei, the internal segment of the globus pallidus (GPi), has been characterized in detail in intact and parkinsonian animals, but the neuronal activity in the second major basal ganglia output nucleus, the substantia nigra pars reticulata (SNr), has received far less attention. This study in primates represents a comparison of the effects of parkinsonism, induced by injections of the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), on the neuronal discharge in the GPi and SNr. These electrophysiologic recording experiments were carried out in three African green and two rhesus monkeys. One hundred and twenty-four neurons were recorded in the GPi before treatment with MPTP, and 93 neurons thereafter. In the SNr, 55 cells were recorded before treatment with MPTP, and 41 cells thereafter. MPTP induced a non-significant increase in the average discharge rate and a significant decrease in the median interspike interval length (ISI) in the GPi (by 13%), whereas no changes were detected in either parameter in the SNr. The average ISI distributions were markedly asymmetric in both structures, and could be modeled by a logarithmic normal distribution. With the MPTP treatment, the mode of the ISI distribution fell by 24% in the GPi (P≤0.01), whereas it did not change significantly in the SNr. An algorithm that detects burst discharges in the raw ISI data (based on the method by Legendy and Salcman) detected a significant increase in the proportion of action potentials that participated in bursts of discharge in both structures (increase by 257% in the GPi, and by 67% in the SNr). Power spectral and autocorrelation analysis revealed that treatment with MPTP increased the proportion of cells with oscillatory burst patterns at 3–8 Hz in both structures (from 0.8% to 27% of all neurons in the GPi, and from none to 10% in the SNr). The results show that neuronal discharge in the SNr is affected in parkinsonism, but that the changes in the SNr are less pronounced then those seen in the GPi.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 223-224 (July 1996), p. 151-160 
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1106
    Keywords: Superior colliculus ; Met-Enkephalin ; Cholinoceptors ; Atropine ; Hexamethonium ; Rabbit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This report presents evidence for the depolarization-dependent release of met-enkephalin from the superior colliculus of the rabbit. Collicular tissue was placed in superfusion chambers and met-enkephalin accumulation in the superfusate was measured by radioimmunoassay. Exposure to high potassium concentrations (30 mM and 56 mM) increased met-enkephalin release. This is the fourth transmitter shown to be released from collicular tissue. Furthermore, we have obtained the first evidence that suggests that metenkephalin release is susceptible to muscarinic modulation. While the depolarization-dependent release of met-enkephalin was depressed in the presence of atropine (1 μM), hexamethonium (100 μM) did not block the increase of met-enkephalin release induced by high potassium.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 325 (1984), S. 124-130 
    ISSN: 1432-1912
    Keywords: Neurotransmitter release ; Caudate nucleus ; Verapamil ; Diltiazem ; Ryosidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Slices of the rabbit caudate nucleus were preincubated with 3H-dopamine or 3H-choline and then superfused with label-free medium. Release of 3H-dopamine and 3H-acetylcholine was elicited by either electrical stimulation at 8 (in one series 2) Hz, or an increase in the K+ concentration by 50 mmol/l, or addition of L-glutamate 1 mmol/l. Verapamil 1 μmol/l, diltiazem 1 and 10 μmol/l, and ryosidine 1 μmol/l failed to the reduce the electrically-, K+- and glutamate-evoked overflow of tritium. Verapamil 1 μmol/l and diltiazem 10 μmol/l also failed to reduce the electricallyevoked overflow (2 Hz) when dopamine receptors, neuronal dopamine uptake, and neuronal choline uptake were blocked by domperidone, nomifensine and hemicholinium, respectively. Inhibition of the evoked overflow of tritium was only obtained when concentrations were increased to verapamil 10 μmol/l, diltiazem 100 μmol/l and ryosidine 10 μmol/l. The inhibition was generally small. It was more evident for slices preincubated with 3H-choline than for those preincubated with 3H-dopamine, because in the latter verapamil, diltiazem and (much less) ryosidine accelerated the basal efflux of tritium. The inhibition of the K+-evoked overflow of tritium was probably due to blockade of Ca2+ channels because this overflow was Ca2+-dependent but tetrodotoxin-resistant. In contrast, the inhibition of the electrically- and glutamateevoked overflow possibly involved blockade of Na+ channels as well. The results indicate that three calcium antagonists from different chemical classes are very weak inhibitors of Ca2+ entry into, and hence transmitter release from, the terminal axons of central dopaminergic and cholinergic neurones. The function of the high affinity calcium antagonist binding sites that have been identified in brain remains unknown.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 46 (1968), S. 438-442 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Anamnesis, findings and clinical course of a patient twenty six years old with typical symptoms of acute intermittend porphyria are represented. The cytological examination showed the normal diploid number 2n=44+XY. The high portion of metaphases with aberrations of chromosomes is especially noted. Among the aberrations of chromosomes breaks of chromosomes and chromatids were especially frequent. Rarefactions, achromasia and entspiralisation were not so frequent. There were still less acentric fragments and dicentric chromosomes. A possible cause is the disturbance of porphyria-metabolism, especially the increase of pathological intermediate products of porphyrin-metabolism. The cytological results of the clinical healthy daughter were normal.
    Notes: Zusammenfassung Anamnese, Befund und klinischer Verlauf eines 26jährigen Patienten mit den typischen Symptomen der akuten intermittierenden Porphyrie werden dargestellt. Die cytologische Untersuchung ergab die normale Diploidzahl von 2n=44+XY. Auffällig war der hohe Anteil von Metaphasen mit Chromosomenaberrationen, unter denen Chromosomen-und Chromatidbrüche gehäuft auftraten, weniger zahlreich reich Verdünnungen, Achromasie sowie Entspiralisation und nur vereinzelt azentrische Fragmente und dizentrische Chromosomen. Als mögliche Ursache scheint die Stoffwechselstörung in Betracht zu kommen, wobei die Porphyrine aber auch in Zwischenstufen als mutagene Faktoren anzusehen wären. Damit könnten auch die normalen cytologischen Befunde der klinisch gesunden Tochter in Einklang stehen.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 338 (1988), S. 623-631 
    ISSN: 1432-1912
    Keywords: Striato-striatal grafts ; Ibotenic acid lesions ; 6-Hydroxy-dopamine lesions ; Acetylcholine release ; Dopamine D2-receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tritium accumulation during incubation with 3-H-choline, and the efflux as well as the electrically evoked overflow of tritium during subsequent superfusion, were investigated in slices from unilateral striatal suspension grafts 16 to 20 weeks after implantation into the previously ibotenic acid-lesioned rat striatum. Slices from non-operated animals, from striata contralateral to grafts, and from animals with acute ibotenic acid lesions of the striatum were studied in parallel. The accumulation of tritium and the overflow of tritium in response to electrical stimulation (2 min, 3 Hz) were markedly impaired in acutely lesioned striata. In graft slices, tritium accumulation and the subsequent electrically evoked overflow were greater than in slices obtained after acute lesions, but were still smaller than in non-operated animals or in the contralateral striata. The dopamine D2-receptor agonist quinpirole inhibited the electrically evoked overflow of tritium in grafts, but only to a small extent. The D2-receptor antagonist sulpiride increased, whereas the dopamine uptake inhibitor nomifensine and the dopamine releasing drug amphetamine decreased the evoked overflow in slices from non-operated rats and from striata contralateral to grafts, but had no significant effect in grafts. As in graft slices, the release of acetylcholine in striata from animals in which the mesostriatal dopamine pathway had been lesioned by 6-hydroxy-dopamine was not changed by sulpiride and amphetamine, and was only minimally decreased by nomifensine. Our data show that striato-striatal grafts can partly restore the impaired choline accumulation and acetylcholine release in excitotoxinlesioned striata. Functional D2-receptors are present on graft cholinergic cells, but are not activated by endogenous dopamine under the present in vitro conditions.
    Type of Medium: Electronic Resource
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