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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of medicinal chemistry 29 (1986), S. 1570-1573 
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 28 (1977), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    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: Abstract— Mn2+ caused an 8-to 16-fold stimulation of adenylate cyclase activity in homogenates as well as synaptosomcs. isolated synaptic membranes, and slices prepared from rat brain. The stimulation occurred at low concentrations of Mn2+. with a doubling of activity at 50-60μM. and was unaffected by a 60-fold excess of Mg2+. Whether or not Mg2+ was added, inclusion of a low concentration of Mn2+ reduced, but did not prevent the stimulation of adenylate cyclase caused by dopaminc in homogenates of corpus striatum. In contrast, Ca2+. at a concentration that had little effect on basal cyclase activity, completely prevented the stimulation by dopamine. The increase of cyclase activity produced by Mn2+ in brain homogenates was potentiated by F−. Other ions, notably Hg2+. Pb2+. Cu2+ and Zn2+. in order of decreasing potency, inhibited both basal and Mn2--stimulated cyclase activity. It is proposed that the effect of Mn2+ on adenylate cyclase activity may involve only the catalytic subunit of the enzyme, and that the mechanism is different from that by which either dopamine or F− stimulates the enzyme. These results suggest that the effects of low concentrations of Mn2+ and certain other divalent metal ions on adenylate cyclase activity may be involved in their neuropsychiatrie or other toxic effects, and that such ions may also participate in normal physiological mechanisms involving cyclic nucleotides.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 23 (1974), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —The uptake of l[14C]glutamine by a crude isolated nerve ending fraction of rat brain was found to be linear with time for at least 5 min, profoundly temperature-dependent, apparently half-saturated at a substrate concentration of 0·26 mm, partially inhibited by dinitrophenol and ouabain and elevated [K+], weakly Na+-dependent, poorly inhibited by drugs which block uptake of biogenic amines and more strongly inhibited by glutamic acid (IC50= 0·5mm) than by aspartic acid, GABA, glycine or methionine. The [14C]glutamine taken up appeared to be associated with nerve endings and was released by membrane-disruption; about 20 per cent was associated with free mitochondria. Glutamine, δ-aminolevulinic acid and several other amino acids were poor inhibitors of [3H]GABA-uptake; δ-aminolevulinic acid was a poor inhibitor of [3H]glutamine-uptake, whereas glutamine was a moderately effective competitive inhibitor (Ki= 1 mm). [14C]glutamine and [3H]GABA were released from brain slices by electrical stimulation or 50 mm K+, while labeled δ-aminolevulinic acid, leucine, urea, amphetamine and tyramine were poorly released. [14C]glutamine was not released by unlabeled glutamate or several aromatic amines. We conclude that the neuropsychiatric features of porphyria are not likely due to a ‘false transmitter’ role for δ-aminolevulinic acid although such a role for glutamine in hepatic encephalopathy or other neuropsychiatric diseases should be considered.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 18 (1971), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The hydroxylated phenylethylamines p-tyramine, m-tyramine, octopamine, metaraminol and norepinephrine were accumulated by homogenates of rat brain much more vigorously than β-phenethylamine or amphetamine. The affinity concentrations (Km) for initial (5-min) uptake by homogenates of whole brain were 0.5, 3 and 6 μM for DL-norepine-phrine, p-tyramine and DL-octopamine, respectively. The uptake of these three hydroxylated compounds was much more vigorous in striatal tissue than in cortical tissue, and in both tissues the rate of uptake decreased in the sequence: norepinephrine 〉 tyramine 〉 octopamine. The uptake of these three substances was inhibited by reduced temperature, by lack of glucose, by CN- and DNP, and by desmethylimipramine, cocaine and ouabain. The uptake of norepinephrine and octopamine appeared to require Na+. Pretreatment of rats with reserpine or 6-hydroxydopamine decreased the ability of brain to take up norepinephrine or octopamine. Previously accumulated labelled phenylethylamines migrated in sucrose density gradients with a peak of radioactivity corresponding to an equilibrium position of catecholamine-containing nerve endings. The magnitude of the retention of [3H]amine in this synaptosornal peak decreased in the order: norepinephrine 〉 octopamine 〉 tyramine. The accumulated amines were released by sonic, osmotic and thermal stresses which disrupt neuronal membranes. The presence of a β-hydroxyl group appeared to protect amines from destruction by monoamine oxidase, presumably by virtue of uptake in presynaptic storage vesicles. During superfusion, tyramine and metaraminol appeared to displace [3H]norepinephrine from binding sites in brain slices.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 19 (1972), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Radioactive hydroxylated phenylethylamines were released in vitro by electrical stimulation of minces of brain tissues from several anatomically discrete areas, while labelled urea and amphetamine were poorly released from all regions. Release of [3H]norepinephrine occurred in the order hypothalamus 〉 caudate nucleus ≥ cerebral cortex, thus in parallel with the distribution of endogenous norepinephrine. In contrast, [3H]tyramine was poorly released from cortical tissues but readily released from minces of caudate nucleus or hypothalamus. [3H]Octopamine was released from all areas, but was most readily released from thecaudatenucleus. Results for cerebral cortex were similar to those for coronal slices or minces of whole brain; release occurred in the order: norepinephrine 〉 octopamine 〉 tyramine in all three preparations. We suggest that certain β-hydroxylated phenolic phenylethyl-amines may be released from norepinephrine- or dopamine-containing nerve endings in the brain, and that their non-β-hydroxylated congeners may be released from neurons in which endogenous amines are not β-hydroxylated.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 18 (1971), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Isolated nerve endings were removed from crude homogenates of rat brain by Millipore filters of pore size 0-5-0-8 μm. Synaptosomes containing L-[3H]norepinephrine were incompletely removed from a non-ionic medium by 0-8 μm pore filters, but were nearly quantitatively removed from Krebs’medium, as demonstrated by density gradient subcellular distribution. In suspension, synaptosomes accumulated labelled norepinephrine. Catecholamine uptake was active; it was inhibited by ouabain, imipramine, cocaine, β-phenethylamine and amantadine. Bound norepinephrine was released by a high concentration of K+. Nerve endings trapped on ultrafilters behaved very similarly to synaptosomes suspended in Krebs’medium by actively accumulating norepinephrine and serotonin; they also possessed monoamine oxidase activity and norepinephrine was released from them by increased concentrations of K+. Ultrafiltration provides a simple, rapid method of preparing metabolically active synaptosomes.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 18 (1971), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Radioactive β-hydroxylated phenylethylamines, DL-octopamine and DL-metara-minol, as well as DL-norepinephrine, were released from slices or minces of rat brain in vitro by electrical or ionic depolarizing stimuli. In contrast, labelled D-amphetamine and p-tyramine were poorly released and the release of urea was barely perceptible. Addition of unlabelled L-norepinephrine to an incubating medium led to displacement of previously bound [3H]octopamine and [3H]metaraminol from a synaptosomal preparation. Pretreat-ment of rats with intrathecal 6-hydroxydopamine markedly decreased the ability of slices of their brains to release [3H]norepinephrine and [3H]octopamine. We suggest that certain phenolic β-hydroxylated phenylethylamines may enter central, norepinephrine-containing nerveendings, may be stored in presynaptic vesicles and may be released by nerve stimulation. Under certain circumstances such compounds may act as neurotransmitters with unknown post-synaptic effects.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Medicine 23 (1972), S. 343-354 
    ISSN: 0066-4219
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine
    Type of Medium: Electronic Resource
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