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  • 1
    Electronic Resource
    Electronic Resource
    Effect of antidepressant and neuroleptic drugs on the electrically evoked release of serotonin from rat cerebral cortex (1987)
    Springer
    Psychopharmacology 91 (1987), S. 175-181 
    Details
    ISSN: 1432-2072
    Keywords: 5-Hydroxytryptamine ; Antidepressants ; Neuroleptics ; Presynaptic receptors ; 5-HT uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of antidepressant and neuroleptic drugs on the electrically evoked release of serotonin (5-HT) was investigated in rat brain cortical slices preincubated with 0.1 μmol/l 3H-5-HT. Zimelidine, trazodone, clomipramine, doxepin, and viloxazine (1 μmol/l each) enhanced the electrically-induced 3H overflow by 20–44%. Six other antidepressants and five neuroleptics did not increase the evoked transmitter release. Only trazodone and viloxazine also increased the 3H overflow in experiments in which neuronal 5-HT reuptake was already blocked by 6-nitroquipazine. 5-HT and clonidine inhibited the electrically-induced 3H-5-HT release by stimulation of presynaptic 5-HT autoreceptors and α2-adrenoceptors, respectively; trazodone and viloxazine had no effect on the concentration-response curves of 5-HT and clonidine. Other psychotropic agents with well known antiserotonergic activities also failed to block presynaptic 5-HT autoreceptors. It is concluded that zimelidine, clomipramine, and doxepin enhanced the 3H-5-HT overflow by inhibition of neuronal 5-HT uptake, whereas the increase produced by trazodone and viloxazine cannot be explained by reuptake inhibition or interaction with presynaptic receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00217058
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of chronic lithium administration on adrenoceptor binding and adrenoceptor regulation in rat cerebral cortex (1988)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 337 (1988), S. 267-272 
    Details
    ISSN: 1432-1912
    Keywords: Lithium ; β-Adrenoceptors ; α-Adrenoceptors ; Receptor regulation ; Antidepressants
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Lithium (Li) at a concentration, which exerts prophylactic effects in affective disorders is known to alter noradrenaline turnover and the β-adrenoceptor-dependent cAMP accumulation. In the present study the action of chronic Li administration (at least 5 weeks) on agonist and antagonist binding to adrenoceptors and on the regulation of adrenoceptors was investigated in rat cerebral cortex. Li treatment caused a small but significant decrease in the number of β-adrenoceptor binding sites by 10% (3H-dihydroalprenolol binding) leaving the number of α1- and α2-adrenoceptor binding sites (3H-prazosin and 3H-rauwolscine, respectively) unchanged. The affinity of the radioligands as well as the affinity of agonists to these binding sites were not altered. The up-regulation of β-adrenoceptor binding sites produced by repeated reserpine injections was inhibited by 32% in rats treated concomitantly with Li, although the noradrenaline depleting effect of reserpine was not impaired. In contrast, Li treatment had no effect on the up-regulation of β-adrenoceptor binding induced by 6-OH-dopamine, nor did it alter the β-adrenoceptor down-regulation following chronic administration of desipramine. The up-regulation of α1-adrenoceptor binding sites caused by reserpine or 6-OH-dopamine also remained unaffected by Li. It is concluded that chronic Li has limited effects on cortical adrenoceptors and their regulation. The inhibition of β-adrenoceptor up-regulation caused by reserpine may reflect an action of Li on non-adrenergic systems rather than a general “stabilizing” effect on adrenoceptors proposed previously.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168837
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    Paper (German National Licenses)
    Fulltext
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