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  • 11
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 27 (1976), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The synthesis, subcellular distribution and turnover of dopamine β-hydroxylase was studied in organ cultures of rat adrenal medullae and superior cervical ganglia. After exposure to [3H]leucine for 1 or 3 h, the tissues were homogenized at various time intervals and the amount of labelled dopamine β-hydroxylase in different subcellular fractions (cytosol, soluble and membrane-bound fraction of catecholamine storage vesicles) was determined by immunoprecipitation and subsequent electrophoresis. In cultured adrenal medullae, induction of dopamine β-hydroxylase initiated in vivo by administration of reserpine affected both soluble and membrane-bound pools of dopamine β-hydroxylase to a similar extent after pulse-labelling for 1 or 3 h. The half-lives of dopamine β-hydroxylase, which amounted to 6 h for the cytosol, 7.5 h for the soluble vesicular and 32 h for the membrane-bound vesicular pools were not altered by pretreatment with reserpine. In superior cervical ganglia the half-lives of the soluble pools were 2–3 times longer than in the adrenal medulla, whereas the half-life of the membrane-bound fraction was the same as in the adrenal medulla. In both organs the most heavily labelled fraction (both after a pulse of 1 or 3 h) was always that of the vesicular membrane, suggesting that newly-synthesized dopamine β-hydroxylase is immediately incorporated into the storage vesicles and not via release into the cytosol from the site of synthesis. The fact that the half-life of membrane-bound dopamine β-hydroxylase is markedly longer than that of the two soluble pools suggests that the single pools are not only independently supplied by newly-synthesized DBH but there is also no appreciable subsequent exchange between soluble and membrane-bound pools.
    Type of Medium: Electronic Resource
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  • 12
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Developmental Biology 137 (1990), S. 451-455 
    ISSN: 0012-1606
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 13
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 330 (1993), S. 287-292 
    ISSN: 0014-5793
    Keywords: Brain-derived neurotrophic factor ; Differentiation ; Gene expression ; Polymerase chain reaction
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 14
    ISSN: 0014-5793
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 15
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 198 (1986), S. 315-320 
    ISSN: 0014-5793
    Keywords: (Rat peritoneal mast cell, Rat leukemia cell line) ; 12-O-Tetradecanoylphorbol 13-acetate ; Ca^2^+ ; Degranulation ; Nerve growth factor
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 16
    ISSN: 0022-1139
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 17
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 282 (1979), S. 413-414 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] NGF was prepared from submaxillary glands of adult male mice by the method of Bocchini and Angeletti8, as the 2.5S subunit, with the modifications of Suda et al9. The purity of NGF was controlled by SDS gel electrophoresis and its biological activity was determined as described by Fenton10. The ...
    Type of Medium: Electronic Resource
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  • 18
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 264 (1969), S. 32-54 
    ISSN: 1432-1912
    Keywords: Aggressiveness ; MAO-inhibitors ; Thymoleptics ; Catecholamines ; Aggressivität ; MAO-Inhibitoren ; Thymoleptica ; Katecholamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung 1. Kombinierte Behandlung von Ratten mit MAO-Inhibitoren und tricyclischen Thymoleptica führte zu einem Erregungssyndrom mit Aggressivität. Allein gegeben waren MAO-Hemmer und Thymoleptica in dieser Hinsicht wirkungslos. 2. Die MAO-Inhibitoren waren untereinander nicht austauschbar: Phenelzin, Iproniazid und Isocarboxazid, aber nicht Harmalin, Pheniprazin, Pargylin und Tranylcypromin lösten in Kombination mit Imipramin Aggressivität aus. 3. Von sieben Thymoleptica riefen nur Imipramin und Amitriptylin, kombiniert mit Isocarboxazid, Aggressivität hervor; Cocain war wirkungslos, Amphetamin führte erst nach Isocarboxazid zu Aggressivität. 4. dl-DOPA erzeugte ohne und mit MAO-Hemmung Aggressivität, 5-Hydroxytryptophan war wirkungslos. Inhibitoren der Katecholamin-Synthese hemmten die Entstehung der Aggressivität. 5. Katecholamine und nicht 5-Hydroxytryptamin dürften bei der Entstehung der Aggressivität eine Rolle spielen. 6. Zentrale Erregung mit Hyperthermie einerseits und Aggressivität andererseits stehen wahrscheinlich nicht in kausaler Beziehung.
    Notes: Summary 1. The combined treatment of rats with MAO-inhibitors and tricyclic thymoleptics caused a central excitation syndrome with aggressiveness. When given alone, MAO-inhibitors and thymoleptics were inactive in this respect. 2. Only phenelzine, iproniazid, and isocarboxazide elicited aggressiveness when combined with imipramine. Harmaline, pheniprazine, pargyline, and tranylcypromine were inactive. 3. Of seven thymoleptics, only imipramine and amitriptyline caused aggressiveness when given after isocarboxazide. Cocaine was not active. Amphetamine produced aggressiveness after isocarboxazide. 4. Aggressiveness was caused bydl-DOPA with and without MAO inhibition, 5-hydroxytryptophan was inactive. Inhibitors of catecholamine synthesis prevented the aggressiveness. 5. Catecholamines, but not 5-hydroxytryptamine, are supposed to play a part in the mechanism leading to aggressiveness. 6. Central excitation with hyperthermia on one hand, and aggressiveness on the other hand are probably not causally related.
    Type of Medium: Electronic Resource
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  • 19
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 264 (1969), S. 326-326 
    ISSN: 1432-1912
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 20
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 289 (1975), S. 157-170 
    ISSN: 1432-1912
    Keywords: Hypophysectomy ; cAMP ; Carbamylcholine ; Dopamine ; Adrenal Medulla ; Tyrosine Hydroxylase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It was the aim of this study to investigate the mechanisms responsible for changes in 3′,5′-cyclic adenosine monophosphate (cAMP) in the rat adrenal medulla occuring after administration of carbamylcholine, histamine, ACTH and various phenylethylamines. Carbamylcholine, ACTH, histamine, noradrenaline and dopamine produced marked (500–900%) increases in adrenal cAMP which were very similar in both adrenal cortex and medulla both with respect to time-course and relative extent. Interestingly isoprenaline and adrenaline did not influence cAMP levels even at excessively high doses. In all cases studied transsection of the splanchnic fibers supplying the adrenals reduced the increase in medullary cAMP by not more than 25–30%, suggesting that cAMP levels in the adrenal medulla are predominantly regulated by non-neuronal mechanisms. This assumption was strongly supported by the observation that hypophysectomy completely abolished the 500–600% increase in cAMP produced by 50 μmol/kg of dopamine and reduced the 700% increase resulting from 4.4 μmol/kg of carbamylcholine to 70%. In spite of the marked increase in cAMP produced by single and repeated doses of dopamine in the adrenal medulla there was no subsequent induction of tyrosine hydroxylase (TH). Moreover carbamylcholine (8.2 μmol/kg) evoked TH induction only in innervated adrenals whereas after denervation, in spite of the large (+500%) and prolonged (more than 90 min) increase in cAMP, no TH induction could be observed. It is concluded that adrenal medullary cAMP is predominantly regulated by the pituitary gland via the adrenal cortex and only to a much smaller extent — if at all—by direct cholinergic mechanisms, which are responsible for the initiation of TH induction.
    Type of Medium: Electronic Resource
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