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  • 1
    Electronic Resource
    Electronic Resource
    Endogenous Noradrenaline Activates α2-Adrenoceptors on Serotonergic Nerve Endings in Human and Rat Neocortex (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Slices from human neocortex preincubated with [3H]serotonin ([3H]5-HT) were superfused and stimulated electrically to investigate whether the α2-adrenoceptors on serotonergic terminals can be stimulated by endogenous noradrenaline (NA) released from neighboring noradrenergic fibers. The stimulation-evoked 3H overflow, representing action potential-induced, exocytotic release of 5-HT, was depressed by the NA uptake blocker (+)-oxaprotiline. Rauwolscine (a mixed α2-adrenoceptor antagonist/5-HT autoreceptor agonist) or phentolamine [a combined α- adrenoceptor/5-HT autoreceptor antagonist; the latter drug in the presence of (+)-oxaprotiline] enhanced the release when the 5-HT autoreceptors had previously been blocked by metitepine. Under hypothermia the release of 5-HT was found to be decreased and that of NA to be increased; under these conditions idazoxan (an α2-adrenoceptor antagonist) enhanced the release of 5-HT. In neocortex slices from rats (+)-oxaprotiline similarly depressed the release of 5-HT (measured with the same methods) as in human tissue. When rats were pretreated with 6-hydroxydopamine, the inhibitory effect of exogenous NA on 5-HT release was increased, and in slices from rats pretreated with desipramine, it was decreased. In conclusion, α2-heteroreceptors can be activated by endogenous NA released from neighboring noradrenergic fibers. Because regulatory processes analogous to those in rats probably occur in humans as well, an up- or down-regulation of α2- heteroreceptors in depressed patients with a (pathological) decrease or a (therapeutic) enhancement of the noradrenergic neurotransmission may also be assumed to occur.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb02148.x
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  • 2
    Electronic Resource
    Electronic Resource
    Mice transgenic for exon 1 of Huntington's disease: properties of cholinergic and dopaminergic pre-synaptic function in the striatum (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 85 (2003), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In Huntington's disease (HD), neuronal loss is most prominent in the striatum leading to emotional, cognitive and progressive motor dysfunction. The R6/2 mice, transgenic for exon 1 of the HD gene, develop a neurological phenotype with similarities to these features of HD. In striatal tissue, electrically evoked release of tritiated acetylcholine (ACh) and dopamine (DA) were compared in wild-type (WT) and R6/2 mice. In R6/2 mice, the evoked release of ACh, its M2 autoreceptor-mediated maximum inhibition and its dopamine D2 heteroreceptor-mediated maximum inhibition was diminished to 51%, 74% and 87% of controls, respectively. Also, the activities of choline acetyltransferase and of synaptosomal high-affinity choline uptake decreased progressively with age in these mice. In the DA release model, however, electrical stimulation elicited equal amounts of [3H]-DA both in WT and R6/2 mice. Moreover, high-affinity DA uptake into striatal slices was similar in WT and R6/2 mice. In order to confirm these findings in vivo, intrastriatal levels of extracellular DA were measured by intracerebral microdialysis in freely moving mice: striatal DA levels were found to be equal in WT and R6/2 mice. In conclusion, in the transgenic R6/2 mice changes occur mainly in striatal cholinergic neurones and their pre-synaptic modulation, but not in the dopaminergic afferent terminals. Whether similar events also contribute to the pathogenesis of HD in humans has to be established.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2003.01704.x
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  • 3
    Electronic Resource
    Electronic Resource
    Opioid receptor-mediated control of acetylcholine release in human neocortex tissue (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 586-592 
    Details
    ISSN: 1432-1912
    Keywords: Key words Acetylcholine release ; Human neocortex ; Opioid receptors ; Endogenous opioids ; Interneurons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of various opioid receptor agonists and antagonists on evoked acetylcholine release were studied in slices of human neocortex prelabelled with [3H]-choline, superfused and depolarized electrically (2 min, 3 Hz, 2 ms, 24 mA) or by K+ (20 mM). The δ-opioid receptor agonist DPDPE and the κ-opioid receptor agonist U50488 reduced the evoked [3H]-overflow (acetylcholine release) in a concentration-dependent fashion; the δ-opioid receptor antagonist naltrindole and the the κ-opioid receptor antagonist norbinaltorphimine, respectively, antagonized these effects. Application of the μ-opioid receptor agonist DAGO also resulted in an inhibition of acetylcholine release; however, both δ- and κ-opioid receptor antagonists were able to block this effect. The μ-opioid receptor agonists morphine and (+)-nortilidine had no effect. These results indicate that acetylcholine release in human neocortex is inhibited through δ- and κ-opioid receptors, but not through μ-opioid receptors. Acetylcholine release was significantly increased by the δ-opioid receptor antagonist naltrindole in the presence of a mixture of peptidase inhibitors providing evidence for a δ-opioid receptor-mediated inhibition of acetylcholine release by endogenous enkephalin. K+-evoked acetylcholine release in the presence of TTX was inhibited by U50488, but not by DPDPE, suggesting the presence of κ-opioid receptors on cholinergic terminals and the localization of δ-receptors on cortical interneurons. Therefore, the potent effect of DPDPE on acetylcholine release is likely to be indirect, by modulation of intrinsic cortical neurons. These interneurons probably do not use GABA as neurotransmitter since both GABAA and GABAB receptor agonists (muscimol and baclofen, respectively) were without effect on acetylcholine release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170832
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  • 4
    Electronic Resource
    Electronic Resource
    Theophylline relieves headache following lumbar puncture (1986)
    Springer
    Journal of molecular medicine 64 (1986), S. 216-218 
    Details
    ISSN: 1432-1440
    Keywords: Headache ; Lumbar puncture ; CSF pressure ; Theophylline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a study of 11 patients with typical headache following diagnostic lumbar puncture the effect of peroral treatment with theophylline (Euphyllin retard) was compared with that of placebo. When the headache was provoked by orthostatic strain, the six patients in the verum group showed significantly less pain (mean pain score: 16±3.91) than the five patients in the placebo group (mean pain score: 28±4.73). This beneficial effect of theophylline on post-puncture headache was subsequently confirmed by open observations of ten additional patients. In view of the small sample size our results should be considered preliminary. Nevertheless, they suggest that additional trials on the benefit of methylxanthines in the treatment of post-puncture headache are called for.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01711650
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  • 5
    Electronic Resource
    Electronic Resource
    Mathematical analysis of the control of neurotransmitter release by presynaptic receptors as a supplement to experimental data (1999)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 359 (1999), S. 345-359 
    Details
    ISSN: 1432-1912
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The quantitative analysis of receptor-mediated effects is based on experimental concentration-response curves in which an independent variable, the concentration of a receptor ligand, is linked with a dependent variable, the biological response. The steps that intervene between the ligand-receptor interaction and the subsequent biologic effect, i.e. modulation of transmitter release in our examples, are largely unknown. Nevertheless, the shape of a concentration-response curve may give some insights into the nature of the relation between receptor occupancy and ensuing response. The shape of the concentration-response curve can be evaluated by nonlinear regression analysis of the data points of the independent and dependent variable. If possible, the model applied should be mechanistically derived from a physical or chemical law, underlying the biological condition. For instance, the inherence of the Law of Mass Action allows to call the model mechanistic. The presence of spare receptors for an agonist must induce an alteration of the shape of the concentration-response curve as compared to a symmetric bimolecular concentration-binding curve. Evaluation methods which neglect the alteration of the geometrical form of concentration-response curves due to non-proportionality between receptor occupation and relative response do not seem appropriate to quantify spare receptors. The “general response function” may allow a mechanistic interpretation of the occupancy-response relationship. This function estimates roughly the number of “non-spare” receptors and of spare receptors on a functional unit that contribute to the response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005361
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  • 6
    Electronic Resource
    Electronic Resource
    Opioid receptor-mediated control of acetylcholine release in human neocortex tissue (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 586-592 
    Details
    ISSN: 1432-1912
    Keywords: Acetylcholine release ; Human neocortex ; Opioid receptors ; Endogenous opioids ; Interneurons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of various opioid receptor agonists and antagonists on evoked acetylcholine release were studied in slices of human neocortex prelabelled with [3H]-choline, superfused and depolarized electrically (2 min, 3 Hz, 2 ms, 24 mA) or by K+ (20 mM). The δ-opioid receptor agonist DPDPE and the κ-opioid receptor agonist U50488 reduced the evoked [3H]-overflow (acetylcholine release) in a concentration-dependent fashion; the δ-opioid receptor antagonist naltrindole and the the κ-opioid receptor antagonist norbinaltorphimine, respectively, antagonized these effects. Application of the μ-opioid receptor agonist DAGO also resulted in an inhibition of acetylcholine release; however, both δ- and κ-opioid receptor antagonists were able to block this effect. The μ-opioid receptor agonists morphine and (+)-nortilidine had no effect. These results indicate that acetylcholine release in human neocortex is inhibited through δ- and κ-opioid receptors, but not through μ-opioid receptors. Acetylcholine release was significantly increased by the δ-opioid receptor antagonist naltrindole in the presence of a mixture of peptidase inhibitors providing evidence for a δ-opioid receptor-mediated inhibition of acetylcholine release by endogenous enkephalin. K+-evoked acetylcholine release in the presence of TTX was inhibited by U50488, but not by DPDPE, suggesting the presence of κ-opioid receptors on cholinergic terminals and the localization of δ-receptors on cortical interneurons. Therefore, the potent effect of DPDPE on acetylcholine release is likely to be indirect, by modulation of intrinsic cortical neurons. These interneurons probably do not use GABA as neurotransmitter since both GABAA and GABAB receptor agonists (muscimol and baclofen, respectively) were without effect on acetylcholine release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170832
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  • 7
    Electronic Resource
    Electronic Resource
    The slope parameter of concentration-response curves used as a touchstone for the existence of spare receptors (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 356 (1997), S. 283-292 
    Details
    ISSN: 1432-1912
    Keywords: Key words Noradrenaline release ; Rat neocortex ; Presynaptic autoinhibition ; Receptor reserve ; Spare receptors ; Model of receptor agonism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present work was stimulated by findings of a large reserve of presynaptic α2-autoreceptors in rat neocortex by different investigators and our own group, using classical models of receptor agonism. The mathematical background of these classical models seems erroneous since the asymmetry that spare receptors introduce into concentration-response curves is not considered appropriately. This asymmetry leads to a steepening of curve fits based on the logistic function. Therefore, the slope parameter c of a logistically fitted concentration-response curve can be used as a touchstone for the existence of spare receptors. Spare receptors induce a c 〉 1. Concentration-response data of the α2-autoreceptor-mediated inhibition of evoked [3H]-noradrenaline release in rat neocortex slices were re-analysed. The estimates of the slope parameter c of logistically fitted concentration-response curves obtained after treatment of rats with either vehicle or N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) to achieve an irreversible inactivation of α2-autoreceptors, were not compatible with the existence of a large receptor reserve. A model for nonlinear regression analysis developed under the a priori assumption of spare receptors confirmed the absence of spare receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005052
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  • 8
    Electronic Resource
    Electronic Resource
    Modulation of cortical acetylcholine release by serotonin: the role of substance P interneurons (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 618-626 
    Details
    ISSN: 1432-1912
    Keywords: Key words ACh release ; Hippocampal formation ; Substance P interneurons ; 5-HT1B receptors ; 5-HT2 receptors ; NK1 receptors ; Alzheimer‘s disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cholinergic system exerts an important modulatory effect on hippocampal functions. Presynaptic inhibition of hippocampal and neocortical acetylcholine (ACh) release by serotonin (5-HT) has been reported in both rat and human brain. There is some controversy, however, concerning the 5-HT receptor which mediates the inhibitory effects of 5-HT. Using slices of the hippocampal formation of rat prelabelled with [3H]-choline, superfused and depolarized electrically (2 min, 3 Hz, 2 ms, 24 mA) or by K+ (20 mM) we observed that 5-HT inhibits hippocampal and entorhinal [3H]-overflow ([3H]-ACh release) by 5-HT1B receptors located on cholinergic terminals. However, this inhibition requires the functional elimination of substance P/γ-aminobutyric acid (SP/GABA) interneurons which express 5-HT2A receptors as shown by in situ hybridisation histochemistry. Activation of these somadendritically located 5-HT2A receptors facilitates SP release. SP, in turn, stimulates hippocampal [3H]-ACh release through NK1 receptors present on cholinergic terminals. These findings suggest close links between cholinergic afferents, SP interneurons and 5-HT2 receptors. A loss of cholinergic afferents and 5-HT2 receptors, along with a reduction in substance P-immunoreactive neurons, have been observed in the brains of patients suffering from Alzheimer‘s disease, suggesting the concept that these three alterations reflect a disruption of a functional unit. The present findings might help to explain early pathological changes in Alzheimer‘s disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170837
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  • 9
    Electronic Resource
    Electronic Resource
    Strychnine-sensitive glycine receptors inducing [3H]-acetylcholine release in rat caudatoputamen: a new site of action of ethanol? (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 356 (1997), S. 738-745 
    Details
    ISSN: 1432-1912
    Keywords: Key words [3H]-Acetylcholine release ; Rat ; caudatoputamen ; Cholinergic interneurons ; Glycine ; receptors ; Serine ; Strychnine ; Ethanol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the present study acute effects of ethanol on [3H]-acetylcholine ([3H]-ACh) release induced by activation of strychnine-sensitive glycine receptors in superfused slices of rat caudatoputamen were investigated. The glycine-evoked [3H]-ACh release (lg EC50 = –4.10, CI95 = [–4.14, –4.05]) was inhibited by strychnine in a competitive manner (pA2 = 6.86, CI95 = [6.61, 7.08]). Release of [3H]-ACh could also be induced by L-serine. L-serine was less potent than glycine (lg EC50 = –2.61, CI95 = [–2.69, –2.52]). Both glycine and L-serine showed similar maximum effects (Emax(glycine) = 1.34, CI95 = [1.24, 1.45]; Emax(L-serine) = 1.19, CI95 = [1.09, 1.32]). Ethanol at concentrations of 2‰ (= 34 mM) and 4‰ (= 68 mM) inhibited glycine-evoked [3H]-ACh release in a manner like the competitive antagonist strychnine, however with lower potency. The pA2 of ethanol was 1.19, CI95 = [0.85, 1.41], at 2‰ [v/v] and 1.51, CI95 = [1.19, 1.78] at 4‰ ethanol. Similar to its action on glycine-evoked [3H]-ACh release, ethanol at 4‰ [v/v] also inhibited L-serine-evoked transmitter release in a competitive-like fashion (pA2 = 0.83, CI95 = [–0.15, 1.18]). We conclude, that strychnine-sensitive glycine receptors, mediating [3H]-ACh release in the rat caudatoputamen, might represent a new site of action of ethanol.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005112
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  • 10
    Electronic Resource
    Electronic Resource
    Why do some antidepressants promote suicide? (1986)
    Springer
    Psychopharmacology 90 (1986), S. 422-422 
    Details
    ISSN: 1432-2072
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00179204
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