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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 301-305 
    ISSN: 1432-1912
    Keywords: Modulation of histamine release ; Dopamine D1-, D2-, D3-receptors ; Hypothalamus ; Push-pull cannula
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The involvement of dopaminergic neurons of the hypothalamus in the modulation of histamine release was studied by the push-pull technique. The posterior hypothalamus of the conscious, freely moving rat was superfused with artificial cerebrospinal fluid (CSF) and the release of histamine was determined radioenzymatically in the superfusate. Agonists and antagonists of dopamine D1-, D2- and D3-receptors were dissolved in CSF and applied to the hypothalamus through the push-pull cannula. Hypothalamic superfusion with the D1-, D2- and D3-receptor agonists dopamine or R(−)-apomorphine enhanced the release rate of histamine. (±) Apomorphine also enhanced the release of histamine, but to a lesser extent than did equimolar concentration of R(−)apomorphine. The D3-agonist quinpirole inhibited the release of histamine, while the D1-receptor agonist SKF 82958 [(±)-6-chloro-7,8-dihydroxy-3-allyl-l-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine] did not virtually influence the release of the neurotransmitter. On the other hand, [−]-sulpiride which predominantly blocks D2-receptors, decreased histamine release. Hypothalamic superfusion with SKF 83566 [(±)-7-bromo-8-hydroxy-3-methyl-l-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine], which seems to be a selective antagonist of D1-receptors, enhanced the release rate of histamine. These findings suggest that dopaminergic neurons of the hypothalamus influence the release of histamine from its neurons in a dual way. D2-heteroreceptors stimulate the release of histamine, while D3-heteroreceptors seem to inhibit the release of this neurotransmitter. Both types of dopamine receptors might be located presynaptically on histaminergic neurons. Alternatively, D3- and D2-receptors might be located on histaminergic and non-histaminergic neurons, respectively.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 33 (1991), S. 129-130 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The hypothalamus of conscious, freely moving rats was superfused with artificial CSF through push-pull cannulae and the release of endogenous histamine was determined radioenzymatically in the superfusate. Superfusion with potassium chloride enhanced the release rate of histamine. The effect of potassium chloride was abolished by α-fluoromethylhistidine. Noradrenaline (α1- and α1-agonist) and clonidine (α2-agonist) decreased the release rate of histamine and inhibited the potassium-induced histamine release. In preliminary experiments, yohimbine (α2-agonist) seemed to increase the release rate of histamine in the superfusate. β-Agonists and antagonists (isoprenaline, salbutamol, propranolol) did not influence the release of histamine.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 344 (1991), S. 183-186 
    ISSN: 1432-1912
    Keywords: Push-pull cannula ; Histamine ; Noradrenaline ; Clonidine ; Yohimbine ; Idazoxan ; Conscious rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The modulation of the histamine release from histaminergic neurons by noradrenergic neurons was investigated by the push-pull technique. The posterior hypothalamus of the conscious, freely moving rat was superfused with artificial CSF through a push-pull cannula and the release of endogenous histamine was determined in the superfusate. Hypothalamic superfusion with a potassium-rich CSF enhanced the release rate of histamine. Superfusion with the α2-agonists noradrenaline or clonidine diminished the release rate of histamine. Moreover, clonidine abolished the potassium-induced increase in the histamine release. Superfusion with the α2-antagonists yohimbine or idazoxan enhanced the release rate of histamine. It is concluded that noradrenaline released from noradrenergic neurons of the hypothalamus modulates the release of histamine from histaminergic neurons by stimulating α2-adrenoreceptors located on histaminergic nerve terminals.
    Type of Medium: Electronic Resource
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