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  • 1
    Electronic Resource
    Electronic Resource
    Histochemische Untersuchung der Wirkung von Pharmaka auf die Aufnahme vonα-Methylnoradrenalin in Noradrenalin- und Dopamin-Neuren bei der reserpinisierten Ratte (1969)
    Springer
    Clinical and experimental medicine 151 (1969), S. 241-260 
    Details
    ISSN: 1591-9528
    Keywords: Catecholamines ; Reserpine-resistant uptake of catecholamines ; Inhibition of neuronal uptake of catecholamines ; Tuberoinfundibular dopamine neurons ; Dibenzobicyclooctadien-derivates ; Katecholamine ; Reserpinresistente Katecholamin-Aufnahme ; Hemmung der neuronalen Aufnahme von Katecholaminen ; Tubero-infundi-buläre Dopamin-Neuren ; Dibenzobicyclooctadien-Derivate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Hemmwirkung verschiedener Pharmaka auf die Aufnahme vonα-Methylnoradrenalin (MNA) in Katecholamin-Neuren wurde fluorescenz-histochemisch an der reserpinisierten Ratte in vivo untersucht. Geprüft wurden die Noradrenalin-Axone in Iris, Mesenterialvenen und Vas deferens sowie die Dopamin-Axone der Eminentia mediana des Hypothalamus. In den Noradrenalin-Neuren hemmen mit abnehmender Wirksamkeit folgende Substanzen: Desipramin, Guanethidin, Methylphenidat, Cocain, 1-(3-Methylaminopropyl)-dibenzo [b, e] bioyclo [2.2.2] octadien (34′276-Ba, ein neues Antidepressivum aus der Reihe der Dibenzo-bicyclo-octadiene) und Tripelennamin. In den Dopamin-Neuren hemmen von diesen Substanzen nur Methylphenidat, Cocain und Tripelennamin. Zwei weitere untersuchte Verbindungen, das Psychopharmakon Benzoctamin (ein Tranquillizer aus der Reihe der Dibenzo-bicyclo-octadiene) und der Monoaminoxydasehemmer N-methyl-N-(2-propinyl)-1-indanamin (11′739-Su) hemmen weder in den Noradrenalin- noch in den Dopamin-Neuren. Mögliche Beziehungen zwischen apparenter Aufnahmehemmung und Entleerung von MNA werden diskutiert.
    Notes: Summary A number of drugs were tested in histochemical studies using a fluorescent technique in order to establish whether they inhibited the uptake ofα-methylnoradrenaline in catecholamine neurones in the reserpine-treated rat in vivo. The noradrenaline axons in the iris, mesenteric veins, and vas deferens were investigated, as well as the dopamine axons of the eminentia mediana of the hypothalamus. In the noradrenaline neurones an inhibitory action was exerted by the following substances (listed in descending order of effectiveness): desipramine, guanethidine, methylphenidate, cocaine, 1-(3-methylaminopropyl)-dibenzo [b, e] bicyclo [2.2.2] octadiene (34′276-Ba, a new antidepressive from the series of the dibenzo-bicyclo-octadienes), and tripelennamine. Of these substances only methylphenidate, cocaine, and tripelennamine exerted an inhibitory effect in the dopamine neurones. Two other compounds that were studied, the psycho-active drug benz-octamine (a tranquillizer from the series of the dibenzo-bicyclo-octadienes) and the monoamine oxidase inhibitor N-methyl-N-(2-propynyl)-1-indanamme (11′739-Su) did not exert an inhibitory effect either in the noradrenaline or in the dopamine neurones. Possible correlations between apparent inhibition of uptake and depletion ofα-methylnoradrenaline are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02044567
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  • 2
    Electronic Resource
    Electronic Resource
    Fluorescence microscopical study of 5-hydroxytryptamine storage organelles in mepacrine-incubated blood platelets of beige mice (Chediak-Higashi syndrome) (1978)
    Springer
    Cellular and molecular life sciences 34 (1978), S. 663-664 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The number and fluorescence intensity of fluorescent granules (5-HT storage organelles) of mepacrine-incubated blood platelets of beige mice (Chediak-Higashi syndrome) are decreased compared to those of control mice platelets. This indicates both quantitative and qualitative changes of the 5-HT organelles, namely a reduced number and a reduced storage capacity, respectively.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01937020
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  • 3
    Electronic Resource
    Electronic Resource
    Flashing phenomenon in blood platelets stained with fluorescent basic drugs (1975)
    Springer
    Cellular and molecular life sciences 31 (1975), S. 593-595 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Zusammenfassung Nach Behandlung von Blutplättchen mit Mepacrin, Acridin-Orange und Daunomycin, die sich selektiv in den 5-Hydroxytryptamin- (5HT)-Speicher-organellen anreichern, werden letztere im Fluoreszenzmikroskop sichtbar. Unter violett-blauer Bestrahlung zeigen die einzelnen Plättchen mehrere sukzessive, blitzartige Zunahmen der Fluoreszenz-Intensität, wobei sie während einiger Sekunden vollständig ausgeleuchtet erscheinen. Die Blitze sind wahrscheinlich durch Freisetzung der fluoreszierenden Stoffe aus je einer 5HT-Speicherorganelle bedingt.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01932478
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  • 4
    Electronic Resource
    Electronic Resource
    Nerve growth factor antagonizes the neurotoxic action of capsaicin on primary sensory neurones (1983)
    [s.l.] : Nature Publishing Group
    Nature 301 (1983), S. 515-517 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] NGF (2.5 S) was prepared from submaxillary glands of adult male mice according to the method of Bocchini and Angeletti17. Capsaicin (Sigma) was dissolved in 10% ethanol-10% Tween-80 (v/v) in 0.9% (w/v) saline. Pregnant Sprague-Dawley rats were housed singly in transparent plastic cages on a 12-h ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/301515a0
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of clonidine on the rate of noradrenaline turnover in discrete areas of the rat central nervous system (1983)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 323 (1983), S. 307-314 
    Details
    ISSN: 1432-1912
    Keywords: Central α1-adrenoceptors ; Central α2-adrenoceptors ; Central noradrenaline neurones ; Central noradrenaline turnover ; Clonidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Turnover of noradrenaline in various regions of the rat brain was estimated by the decrease in noradrenaline content and/or formaldehyde-induced catecholamine fluorescence after inhibition of noradrenaline biosynthesis with α-methyl-p-tyrosine. Clonidine (0.1 and 0.3 mg/kg p.o.) decelerated the decrease in noradrenaline content of the locus coeruleus, the nucleus of the solitary tract, the intermediolateral cell column and the ventral horn of the thoracic spinal cord, as measured in tissue punches of the respective regions with a sensitive radioenzymatic method. In all these central regions the clonidine-induced decrease in noradrenaline turnover was antagonized by yohimbine, but not by phenoxybenzamine, indicating mediation through central α2-adrenoceptors, similar to the cardiovascular effects clonidine. When given alone, both yohimbine and phenoxybenzamine accelerated the disappearance of noradrenaline after inhibition of its biosynthesis. The combined results of radioenzymatic assay and fluorescence histochemistry determinations demonstrated that clonidine markedly reduced noradrenaline turnover in central noradrenaline-containing nerve terminals, but had no effect on the cell bodies of the A1 and A2 cell groups. Noradrenaline turnover was, however, decreased in projection areas of the A1 and A2 cell groups, namely the intermediolateral cell column of the spinal cord and nucleus of the solitary tract, respectively. This observation argues against the existence of a neuronal feedback loop running from the projection areas to the cell bodies of the A1 and A2 cell groups and mediating inhibition of noradrenaline turnover. The effect of clonidine on noradrenaline turnover is, therefore, most likely the result of a local feedback inhibition through presynaptic α-adrenoceptors. Since the nucleus of the solitary tract and the intermediolateral cell column of the spinal cord are prime candidates for the site of the cardiovascular action of clonidine and since the cardiovascular effects of clonidine can be elicited in the virtual absence of neuronal noradrenaline (Haeusler 1974), the present results suggest that the decrease in central noradrenaline turnover and the cardiovascular effects of clonidine are not interrelated phenomena.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00512468
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  • 6
    Electronic Resource
    Electronic Resource
    Cholinergic but not monoaminergic denervation increases nerve growth factor content in the adult rat hippocampus and cerebral cortex (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 334 (1986), S. 346-351 
    Details
    ISSN: 1432-1912
    Keywords: Nerve growth factor (NGF) ; Rat basal forebrain ; Cholinergic neurons ; Monoaminergic neurons ; Denervation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have investigated whether degeneration of basal forebrain cholinergic neurons is a potential trigger for increased NGF production in the adult rat brain. Electrolytic lesions of cholinergic neurons in the septum-diagonal band and in the nucleus basalis of Meynert induced a transient increase in NGF in the ventral hippocampus (+70%) and cerebral cortex (+125%), respectively. In contrast, selective aminergic denervation of the forebrain by electrolytic lesion of the medial forebrain bundle, did not increase NGF levels in hippocampus and cerebral cortex. Thus, a cholinergic mechanism appears to regulate NGF production in adult rat basal forebrain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00569368
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  • 7
    Electronic Resource
    Electronic Resource
    Biochemistry and pharmacology of moclobemide, a prototype RIMA (1992)
    Springer
    Psychopharmacology 106 (1992), S. S6 
    Details
    ISSN: 1432-2072
    Keywords: MAO-A inhibitor ; Moclobemide ; Antidepressant biochemistry ; Pharmacology ; Monoamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract RIMA is a term for reversible inhibitors of monoamine oxidase (MAO) with preference for MAO-A; moclobemide is a prototype of this new class of antidepressants and is a highly selective inhibitor of MAO-A in vitro. This inhibition is reversible by dialysis in vitro, which accounts for the dose-dependent duration of in vivo enzyme inhibition of 12–24 h. Moclobemide increases the content of serotonin, noradrenaline and dopamine in the brain, and decreases that of their deaminated metabolites. Its biochemical, neurological and behavioural effects indicate that it increases the extracellular concentration of the classic monoamine neurotransmitters/neuromodulators — in particular 5-HT. Potentiation of the cardiovascular effects of tyramine is less pronounced after taking moclobemide than after irreversible MAO-A inhibitors. Understanding of the physiological role of MAO and of the events that link inhibition of the enzyme with modulation of neuronal activities in the CNS remains incomplete. A major physiological role of intraneuronal MAO is to keep cytosolic amine concentration very low, to enable the neuronal monoamine carriers to produce a net inward transport of monoamines, and thereby to act as the first step in the termination of action of extracellular monoamines. MAO is likely to have a similar function in non-monoaminergic cells with respect to the monoamine carriers they contain. In addition to the classic monoamines, “trace” amines may become functionally active after MAO inhibition. An alternative role for MAO is that of a scavenger, preventing natural substrates from accumulating in monoaminergic neurons and interacting with storage, release, uptake and receptor function of monoamines.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02246225
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  • 8
    Electronic Resource
    Electronic Resource
    Absence of dopamine sensitive adenylate cyclase in the A10 region, the origin of mesolimbic dopamine neurones (1979)
    Springer
    Cellular and molecular life sciences 35 (1979), S. 744-746 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Dopamine (DA) failed to stimulate the adenylate cyclase of the mesolimbic A10 DA nerve cell body area, in contrast to its activating effect in the nigrostriatal A9 DA cell body area. The enzyme was stimulated by GMPPNP (a GTP analog) and NaF. This indicates the absence in the A10 cell area of DA receptors with functional coupling on adenylate cyclase, in contrast to the A9 cell area where such DA receptors are believed to be located on afferent axon terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01968219
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  • 9
    Electronic Resource
    Electronic Resource
    Degeneration and regeneration of adrenergic nerves in mesenteric blood vessels, iris and atrium of the rat after 6-hydroxydopamine injection (1975)
    Springer
    Journal of neurocytology 4 (1975), S. 157-176 
    Details
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Degeneration of adrenergic axons after 6-hydroxydopamine (6-OH-DA), 2 × 68 mg kg−1 i.v. within 6 h, and the subsequent regeneration process over the following 205 days were studied in rat mesenteric vessels, right atria and irides, using the histochemical fluorescence method of Falck and Hillarp. The objective of the study was to determine why noradrenaline is less depleted and recovers much more rapidly in the mesentery than in other tissues after 6-OH-DA (Finchet al., 1973). The mesentery was further studied by electron microscopy and noradrenaline content analyses, until day 29 after 6-OH-DA treatment. Virtually all adrenergic terminal axons in these tissues were destroyed one day after 6-OH-DA. The large nonterminal axon bundles which occur along the mesenteric vessels and rarely in the heart survived and revealed an intensified catecholamine fluorescence; correspondingly, the mesenteric noradrenaline content was only reduced to 29% of control values. In contrast, such large nonterminal axon bundles were not observed in control iris preparations, and no adrenergic fibres survived in the irides, as suggested by fluorescence microscopy. Regenerating axons were observed in all organs after 3–8 days. The number of nerve terminals along the circumference of the external elastic lamina, as observed in ultrathin cross sections of mesenteric vessels, appeared virtually normal 4 weeks after treatment. Meanwhile, the noradrenaline content of the mesentery returned to approximately 85% of control values. As suggested by fluorescence microscopy, complete adrenergic regeneration occurred in mesenteric vessels between days 46 and 105, while regeneration in atrium and iris was incomplete even at day 205. The density of adrenergic axons in the iris, morphometrically determined, was only 76% and 88% of controls on days 160 and 205, respectively. The survival of the many large nonterminal axon bundles in the mesentery with increased NA content explains the relatively small NA depletion of the mesentery. The rapid recovery of the mesenteric NA content is due to faster regeneration of adrenergic terminal axons in the mesentery as compared with iris and atrium. This is tentatively explained in terms of sprouting from the large axon bundles surviving close to the destroyed terminal axons of the mesenteric vessels, whereas in the other tissues no (iris) or only a few (atrium) large nonterminal axon bundles occur and persist to act as a source of quickly regenerated terminal axons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01098780
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  • 10
    Electronic Resource
    Electronic Resource
    Distribution of indolealkylamine nerve terminals in the ventricles of the rat brain (1973)
    Springer
    Cell & tissue research 144 (1973), S. 511-522 
    Details
    ISSN: 1432-0878
    Keywords: Cerebral ventricles (rat) ; Supra-ependymal nerves ; Indolealkylamine containing nerves ; Fluorescence histochemistry ; Fine-structural cytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The density, distribution and the pharmacologically produced changes of a formaldehyde-induced yellow supra-ependymal fluorescence in the lateral and third ventricles and in the aqueduct of the rat brain are described. The fluorescence consists of small spots or a thin spotted layer just above the ependymal cells. The highest fluorescence densities occur in the areas near the tela chorioidea of the third ventricle and in the interventricular foramen. A high to moderate density occurs in the lateral ventricles and in the aqueduct. Little or no fluorescence is seen above the hypothalamic areas bordering the third ventricle. The fluorescence rapidly fades upon irradiation with violet-blue light, disappears after treatment of the rats with reserpine or p-chlorophenylalanine, is intensified after nialamide or reserpine + nialamide, and does not change after α-methyl-p-tyrosine. Electron microscopically supra-ependymal varicose nerves containing small (500 Å) and large (1000 Å) vesicles in the varicosities are observed in areas with supra-ependymal yellow fluorescence. A fine-structural cytochemical technique reveals the presence of a specific, chromaffine, reserpine-sensitive electron dense core in the small and large vesicles. The conclusion is drawn that a characteristically distributed population of supra-ependymal efferent nerve terminals containing an indolealkylamine, most probably 5-hydroxytryptamine, exists in the cerebral ventricles of the rat brain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00307377
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