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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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  • 2
    Electronic Resource
    Electronic Resource
    α1-Adrenoceptors of rat myocardium: Comparison of agonist binding and positive inotropic response (1988)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 338 (1988), S. 582-588 
    Details
    ISSN: 1432-1912
    Keywords: Cardiac α1-adrenoceptors ; 3H-Prazosin binding ; Positive inotropic effect ; Temperature sensitivity ; Receptor desensitization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Binding of agonists to al-adrenoceptors labelled by 3H-prazosin was investigated in membranes of rat myocardium and compared to the inotropic response elicited by α1-adrenoceptor activation on isolated right ventricles. 1. At 30°C the full agonists, adrenaline and phenylephrine, displaced 3H-prazosin with a shallow inhibition curve. The data are compatible with the assumption that 32% of the binding sites were in a state of high affinity for the agonist adrenaline (KI 85 nmol/l) and 68% in a low affinity state (KI I738 nmol/l). GTP transformed all binding sites into the low affinity form suggesting that at least some of the cardiac α1-adrenoceptors are coupled to N-proteins. 2. At 0°C most of the binding sites (86%) were in a state of high affinity for agonists (KI for adrenaline: 91 nmol/l). 3. For several partial agonists and antagonists (cirazoline, methoxamine, indanidine (Sgd 101-75), oxymetazoline and phentolamine) no such distinct temperature- and GTP-shifts could be demonstrated suggesting a different kind of interaction with al-binding sites. 4. When temperature was changed during incubation with adrenaline, a rise of temperature (from 0°C to 30°C) converted high affinity sites into the low affinity form, whereas a decrease in temperature (from 30°C to 0°C) failed to induce the high affinity state for agonists. Short term incubation (0.5 min) with adrenaline at 30°C resulted in significantly lower IC50 values as compared to equilibrium conditions at the same temperature. 5. Occupancy of al-adrenoceptor binding sites with adrenaline at O°C but not at 30°C rather closely paralleled the concentration-response curve for the α1-mediated increase in ontractile force. 6. Irreversible blockade of α1-adrenoceptors with phenoxybenzamine decreased the maximum inotropic response but only slightly affected pD2 values for the α1-stimulant effect of adrenaline. Our binding experiments suggest that myocardial α1-adrenoceptors can exist in states of different affinity for agonists. Some agonists like adrenaline and phenylephrine seem to induce a temperature-dependent change in the conformation of the receptor which may represent a rapid form of desensitization. Since no appreciable receptor reserve was detected it is hypothesized that the high affinity state which can be measured at 0°C under equilibrium conditions may be relevant to the initiation of the functional response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00179334
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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