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  • 1
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    German Medical Science; Düsseldorf, Köln
    In:  55. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 1. Joint Meeting mit der Ungarischen Gesellschaft für Neurochirurgie; 20040425-20040428; Köln; DOCP 03.24 /20040423/
    Publication Date: 2004-04-22
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 2
    ISSN: 1432-1106
    Keywords: Key words Human neocortex ; Rat neocortex ; Acetylcholine release ; Autoinhibition ; Alzheimer’s disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  In order to assess the autoinhibitory control of endogenous acetylcholine (ACh) in rat and human neocortex, slices of these tissues were prelabelled with [3H]choline, superfused continuously and stimulated electrically using various frequencies in the presence or absence of drugs. The autoinhibitory feedback control of [3H]ACh release was operative – despite the absence of blockers of ACh esterase – at stimulation frequencies ≥3 Hz in rat and ≥6 Hz in human neocortex tissue. At these frequencies the muscarinic antagonist atropine (0.1 µM) disinhibited the release of [3H]ACh in both species. Estimation of the biophase concentration of ACh near the autoreceptor in the rat neocortex from concentration-response curves of the muscarinic agonist oxotremorine revealed that at 3 Hz about 25% of the autoreceptors were activated by endogenously released ACh. This estimation is consistent with an increase in [3H]ACh release to about 120% of control values by complete blockade of autoreceptors with atropine. The observation that in human neocortical tissue presynaptic autoinhibition of [3H]ACh release is operative at stimulation frequencies ≥6 Hz suggests that selective blockade of autoinhibition may also increase ACh release in the cortex of Alzheimer’s disease patients, without additional blockade of the enzyme acetylcholinesterase.
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  • 3
    ISSN: 1432-2072
    Keywords: Caudate nucleus ; Hippocampus ; Serotonin ; Dopamine ; Chlorimipramine ; Fluvoxamine ; 6-Nitroquipazine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Slices of rabbit hippocampus or caudate nucleus were incubated with [3H]-5-HT (0.1 µM, 60 min) or with [3H]-DA. In hippocampal tissue, the 5-HT uptake blockers chlorimipramine, fluvoxamine, and 6-nitroquipazine (0.1, 1, 10 µM) reduced the percentage content of [3H]-5-HT in a concentration dependent manner. The degree of inhibition of [3H]-5-HT content produced by the 5-HT uptake inhibitors was not affected by the MAO inhibitors pargyline or amezinium (which by themselves enhanced [3H] loading) or the catecholamine uptake inhibitor nomifensine (which by itself did not affect [3H] loading). In caudate nucleus tissue, however, the [3H]-5-HT accumulation was reduced only at the highest concentration of the 5-HT uptake blockers (10 µM). In the additional presence of the MAO inhibitors or nomifensine (which by themselves increased or diminished, respectively, the [3H] labelling) the 5-HT uptake inhibitors became more potent in reducing the percentage [3H]-5-HT accumulation of caudate nucleus slices. These results indicate (1) that a false labelling of [3H]-5-HT into dopaminergic terminals in the caudate nucleus can be prevented by nomifensine, (2) that the 5-HT uptake blockers seem to accumulate within the dopaminergic terminals, where they may display a MAO inhibitory property. The 5-HT uptake blockers were ineffective on the percentage tritium accumulation of caudate nucleus slices incubated with [3H]-DA, regardless of the presence of pargyline or nomifensine. Tritiated DA and deaminated [3H]-metabolites were separated in the superfusate of [3H]-DA-release experiments in caudate nucleus tissue. In the presence of 6-nitroquipazine the percentage efflux of unmetabolized [3H]-DA was significantly enhanced in a concentration and time dependent manner. In comparison to 6-nitroquipazine, fluvoxamine was less potent in that respect. 6-Nitroquipazine inhibited the electrically evoked [3H]-DA and [3H]-ACh release from caudate nucleus slices in a concentration dependent manner. The effects on [3H]-DA release were abolished in the presence of pargyline. The inhibition of [3H]-ACh release was significantly diminished by the D2-receptor antagonist domperidone. In conclusion, some 5-HT-related drugs may diminish the release of ACh from caudate nucleus slices via an enhanced dopaminergic transmission due to inhibition of MAO within the dopaminergic terminals.
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 90 (1986), S. 422-422 
    ISSN: 1432-2072
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 5
    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.
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  • 6
    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.
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  • 7
    ISSN: 1432-1912
    Keywords: Noradrenaline release ; Serotonin release ; Hippocampus ; Dopamine receptors ; α2-Adrenoceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 3H-Noradrenaline release in the rabbit hippocampus and its possible modulation via presynaptic dopamine receptors was studied. Hippocampal slices were preincubated with 3H-noradrenaline, continuously superfused in the presence of cocaine (30 μmol/l) and subjected to electrical field stimulation. The electrically evoked tritium over-flow from the slices was reduced by 0.1 and 1 μmol/l dopamine and apomorphine, but significantly enhanced by 10 μmol/l apomorphine or by 0.1 and 1 μmol/l bromocriptine. If the α2-adrenoceptor antagonist yohimbine (0.1 μmol/l) was present throughout superfusion, the inhibitory effects of dopamine and apomorphine were more pronounced and even 10 μmol/l apomorphine and 1 μmol/l bromocriptine inhibited noradrenaline release. Qualitatively similar observations were made in the presence of another α2-antagonist, idazoxane (0.1 μmol/l). In the presence of the D2-receptor antagonist domperidone (0.1 μmol/l) the inhibitory effects of dopamine were almost abolished, whereas both apomorphine (〉1 μmol/l) and bromocriptine (〉0.01 μmol/l) greatly facilitated noradrenaline release. The D2-receptor agonist LY 171555 (0.1 and 1 μmol/l) significantly reduced the evoked noradrenaline release whereas the D1-selective agonist SK & F 38393 was ineffective at similar concentrations. The effects of LY 171555 were abolished in the presence of domperidone (0.1 μmol/l) but remained unchanged in the presence of yohimbine or idazoxane (0.1 μmol/l, each). At 1 μmol/l the D2-receptor antagonists domperidone and (-)sulpiride significantly increased the evoked noradrenaline release by about 10%. However, at this concentration, domperidone (but not (-)sulpiride) affected also basal tritium outflow. Bulbocapnine and the preferential D1-receptor antagonists SCH 23390 enhanced the evoked noradrenaline release already at 0.1 μmol/l. Their marked facilitatory effects (50 to 60% increase at 1 μmol/l) were reduced in the presence of idazoxane (0.1 μmol/l) and almost abolished in the presence of 0.1 μmol/l yohimbine, whereas the increase due to 1 μmol/l (-)sulpiride persisted under these conditions. The evoked tritium efflux from rabbit hippocampal slices preincubated with 3H-serotonin was not affected by dopamine receptor agonists. From our results we conclude that hippocampal noradrenaline, but not serotonin release, is modulated via D2-dopamine receptors. In addition, our results provide evidence for more or less pronounced α2-adrenoceptor agonistic properties of dopamine and α2-adrenoceptor antagonistic properties of apomorphine, bromocriptine, SCH 23390 and bulbocapnine in this noradrenaline release model from CNS tissue.
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  • 8
    ISSN: 1432-1912
    Keywords: A1 adenosine receptors ; Serotonin release ; Hippocampus ; Caudate nucleus ; Rabbit ; Endogenous adenosine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of A1 adenosine receptor ligands on the evoked release of serotonin (5-HT) were studied in slices of the hippocampus and the caudate nucleus of the rabbit, preincubated with 3H-5-HT. In hippocampal tissue electrical stimulation elicited a release which was inhibited by the adenosine receptor agonist N6-cyclohexyladenosine (CHA) and enhanced by the selective A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). The concentration-response curve of CHA was shifted to the right by DPCPX. The shift corresponded to a pA2 value of 9.4 for DPCPX. CHA, R-N6-phenylisopropyladenosine (R-PIA) and DPCPX were ineffective in caudate nucleus tissue. When instead of electrical pulses high K+ was used to induce 5-HT release in the presence of the Na+ channel blocker tetrodotoxin (TTX), which was present in order to exclude effects mediated by interneurones, CHA was equally effective in the hippocampus but again failed to modify 5-HT release in the caudate nucleus. The disinhibition by DPCPX of the evoked 5-HT release was used to calculate the extracellular concentration of endogenous adenosine at the A1 receptor. The calculation greatly depended on the dissociation constant of adenosine at the A1 receptor. It is concluded that A1 adenosine receptors, activated by the endogenous agonist at a concentration of about 0.7 μmol/l, are located on serotonergic nerve endings in the hippocampus, but not in the caudate nucleus. The estimated extracellular concentration of endogenous adenosine is in reasonable agreement with actually measured concentrations reported in the literature.
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  • 9
    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.
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  • 10
    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.
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