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  • 1
    Electronic Resource
    Electronic Resource
    Para-substituted Phe3 deltorphin analogs: enhanced selectivity of halogenated derivatives for .sigma. opioid receptor sites (1992)
    s.l. : American Chemical Society
    Journal of medicinal chemistry 35 (1992), S. 4651-4657 
    Details
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jm00103a001
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Phe3-substituted analogs of deltorphin C. Spatial conformation and topography of the aromatic ring in peptide recognition by .delta. opioid receptors (1993)
    s.l. : American Chemical Society
    Journal of medicinal chemistry 36 (1993), S. 3748-3756 
    Details
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/jm00076a001
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Topographical conformations of the deltorphins predicate .delta. opioid receptor affinity (1993)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 115 (1993), S. 8503-8504 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja00071a092
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Regulation of nicotinic receptors in the brain of mice withdrawn from chronic oral nicotine treatment (1998)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 357 (1998), S. 176-182 
    Details
    ISSN: 1432-1912
    Keywords: Key words Nicotine ; Nicotinic Receptors ; Withdrawal ; Locomotor ; Depression ; Cortex ; Midbrain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of nicotine withdrawal on regional regulation of brain nicotinic receptors was studied in mice after chronic administration of nicotine in the drinking water for 2, 4 or 7 weeks. Two weeks of chronic nicotine administration did not alter the binding of [3H]-nicotine in the midbrain, cortex or cerebellum of the mice, while after both 4-and 7-week treatments a significant increase in the specific [3H]-nicotine binding was observed in cortical and midbrain membranes. In the midbrain, the [3H]-nicotine binding was increased by about 40% in mice withdrawn for 48–72 h from the 4-week chronic nicotine treatment and in mice withdrawn for 48 h from the 7-week treatment. The [3H]-nicotine binding was significantly increased (by 55–65%) in the cortex at 48 h and 72 h after withdrawal from 4-week chronic nicotine and it was even somewhat more increased (by 72–66%) after 7-week treatment. The cortical [3H]-nicotine binding was not altered at 24 h after the 4-week treatment, but in mice withdrawn for 24 h from the 7-week treatment it was increased by 116%. The increases in [3H]-nicotine binding returned to control levels within 1 week after withdrawal. None of the studied treatments affected the [3H]-nicotine binding in the cerebellum. Tolerance towards nicotine-induced locomotor depression was only found in mice withdrawn for 24 h from the 7-week chronic nicotine administration. These findings suggest that at least 4-week chronic nicotine administration in the drinking water is needed before any upregulation of nicotinic receptors can be observed. Furthermore, in our experiments the increase in the [3H]-nicotine binding was seen before behavioural tolerance could be demonstrated. The differences between brain regions in the time course of nicotinic receptor upregulation may reflect variations in nicotinic receptor subunits and their sensitivity to chronic nicotine treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005152
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  • 5
    Electronic Resource
    Electronic Resource
    Brain histamine H3 receptors in rats with portacaval anastomosis: in vitro and in vivo studies (1998)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 358 (1998), S. 574-581 
    Details
    ISSN: 1432-1912
    Keywords: Key words Portacaval anastomosis ; Brain histamine ; Histamine release ; Histamine H3 receptors ; Autoradiography ; [3H]-R-α-methylhistamine binding ; Thioperamide ; Microdialysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The long-term effects of portacaval anastomosis (PCA) on histamine H3 receptors in rat brain were studied by in vitro and in vivo methods. The overflow of histamine from the anterior hypothalamus and from cortex after long-term PCA was determined by in vivo microdialysis. The binding properties of [3H]-R-α-methylhistamine in membranes from cortex, cerebellum, and rest of brain (ROB) were examined with saturation binding experiments. The regional distribution of [3H]-R-α-methylhistamine binding sites in the brain of sham- and PCA-operated rats was assessed also with autoradiography. The tissue levels of histamine were significantly elevated in cortex and ROB of PCA-operated rats. In addition, the spontaneous and K+-evoked overflow of histamine from anterior hypothalamus, and the thioperamide-induced overflow from both anterior hypothalamus and cortex were increased after chronic PCA. In spite of the significantly elevated tissue concentrations and the moderate increase in histamine release, the binding properties of [3H]-R-α-methylhistamine to cortical membranes were not significantly changed. However, the autoradiography study did reveal a decrease in [3H]-R-α-methylhistamine binding density, particularly in striatum and cortex, where H3 receptors are located mainly at non-histaminergic neurons. In conclusion, we suggest that there is a region-selective increase in the histaminergic activity in chronic PCA, which leads to the down-regulation of somadendritic and pre-synaptic H3 receptors located at non-histaminergic neurons. At the same time, the autoreceptor mediated control of histamine neuronal activity via pre-synaptic H3 receptors located at histaminergic neurons is preserved after long-term PCA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005295
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  • 6
    Electronic Resource
    Electronic Resource
    Withdrawal from repeated morphine sensitises mice to the striatal dopamine release enhancing effect of acute morphine (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 350 (1994), S. 548-554 
    Details
    ISSN: 1432-1912
    Keywords: Key words: Morphine challenge – Morphine withdrawal – Striatal dopamine release – Striatal dopamine metabolites – D1 and D2 dopamine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The effects of morphine withdrawal and challenge on the α-methyl-p-tyrosine (αMT)-induced depletion of dopamine (DA) as well as on DA metabolism and 3H-SCH 23390 and 3H-spiperone binding were studied in the striata of male mice. Morphine was given s.c. 3 times daily for 5 days followed by 1 to 3 days‘ withdrawal.   The αMT-induced DA depletion was retarded in mice withdrawn for 1 day from repeated morphine. At this time point the striatal concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) fell, too. In mice withdrawn for 3 days from morphine neither DA depletion nor DOPAC or HVA concentrations differed from those of control mice. In control mice acute morphine challenge accelerated the DA depletion at the dose 10 mg/kg but not at the dose 30 mg/kg. Both doses elevated striatal DOPAC and HVA. In mice withdrawn from repeated morphine for 1 day acute morphine partially counteracted the withdrawal-induced retardation of DA depletion and elevated striatal DOPAC and HVA clearly less than in control mice. However, in mice withdrawn for 3 days 10 mg/kg of morphine clearly enhanced DA depletion and its effect on striatal HVA was significantly augmented. In these mice as in controls the 30 mg/kg dose did not alter striatal DA depletion and elevated HVA less than in controls. Acute morphine did not alter striatal 3-methoxytyramine (3-MT) concentration in control mice but at the dose 10 mg/kg increased it in mice withdrawn for 3 days. Morphine withdrawal did not significantly affect striatal 3H-SCH 23390 binding, but slightly decreased 3H-spiperone binding in mice withdrawn for 3 days indicating a down-regulation of D2 receptors.   Our results by using three different indices of DA release (DA depletion after αMT, HVA and 3-MT) show that long enough withdrawal from repeated morphine treatment augments the morphine-induced release of striatal DA in mice. We propose that the striatal DA release in mice is regulated by two opposite opioid sensitive mechanisms with different dose-dependencies and different tolerance development.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00173025
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  • 7
    Electronic Resource
    Electronic Resource
    Withdrawal from repeated morphine sensitises mice to the striatal dopamine release enhancing effect of acute morphine (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 350 (1994), S. 548-554 
    Details
    ISSN: 1432-1912
    Keywords: Morphine challenge ; Morphine withdrawal ; Striatal dopamine release ; Striatal dopamine metabolites ; D1 and D2 dopamine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of morphine withdrawal and challenge on the a-methyl-p-tyrosine (αMT)-induced depletion of dopamine (DA) as well as on DA metabolism and 3H-SCH 23390 and 3H-spiperone binding were studied in the striata of male mice. Morphine was given s.c. 3 times daily for 5 days followed by 1 to 3 days' withdrawal. The αMT induced DA depletion was retarded in mice withdrawn for 1 day from repeated morphine. At this time point the striatal concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) fell, too. In mice withdrawn for 3 days from morphine neither DA depletion nor DOPAC or HVA concentrations differed from those of control mice. In control mice acute morphine challenge accelerated the DA depletion at the dose 10 mg/kg but not at the dose 30 mg/kg. Both doses elevated striatal DOPAC and HVA. In mice withdrawn from repeated morphine for 1 day acute morphine partially counteracted the withdrawal-induced retardation of DA depletion and elevated striatal DOPAC and HVA clearly less than in control mice. However, in mice withdrawn for 3 days 10 mg/kg of morphine clearly enhanced DA depletion and its effect on striatal HVA was significantly augmented. In these mice as in controls the 30 mg/kg dose did not alter striatal DA depletion and elevated HVA less than in controls. Acute morphine did not alter striatal 3-methoxytyramine (3-MT) concentration in control mice but at the dose 10 mg/kg increased it in mice withdrawn for 3 days. Morphine withdrawal did not significantly affect striatal 3H-SCH 23390 binding, but slightly decreased 3H-spiperone binding in mice withdrawn for 3 days indicating a down-regulation of D2 receptors. Our results by using three different indices of DA release (DA depletion after aMT, HVA and 3-MT) show that long enough withdrawal from repeated morphine treatment augments the morphine-induced release of striatal DA in mice. We propose that the striatal DA release in mice is regulated by two opposite opioid sensitive mechanisms with different dose-dependencies and different tolerance development.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00173025
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    Paper (German National Licenses)
    Fulltext
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