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  • 1
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    German Medical Science; Düsseldorf, Köln
    In:  Nationaler Workshop im Rahmen des European Clinical Research Infrastructures Network (ECRIN); 20041005-20041005; Frankfurt/Main; DOC04ecrin01 /20041221/
    Publication Date: 2004-12-22
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 2
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of isoprenaline, noradrenaline and fenoterol on the electrically evoked release of [3H]-acetylcholine from the rat phrenic nerve were investigated.2. Isoprenaline (0.1 μmol/L) and noradrenaline (1 μmol/L) enhanced evoked [3H]-acetylcholine release by about 90%, an effect which was abolished by CGP 20712A (0.1 μmol/L), a specific antagonist at β1-adrenoceptors. Noradrenaline still enhanced [3H]-acetylcholine release in the presence of phentolamine (1 μmol/L).3. The enhancing effect of both isoprenaline and noradrenaline decreased at prolonged exposure times (24–32 min). A pre-exposure of the tissue to a low concentration (0.01 μmol/L) of isoprenaline prevented the enhancing effect of 0.1 μmol/L isoprenaline.4. Fenoterol, a specific agonist at β2-adrenoceptors, did not modify evoked [3H]-acetylcholine release.5. The present results indicate the existence of facilitatory β1-adrenoceptors on the motor nerve. These receptors appear to be desensitized either by a high concentration of, or by a long exposure to, agonists. Under the present conditions noradrenaline enhances the release of newly synthesized transmitter mainly by stimulation of β-adrenoceptors.
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  • 3
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Acetylcholine (ACh) represents one of the most exemplary neurotransmitters. In addition to its presence in neuronal tissue, there is increasing experimental evidence that ACh is widely expressed in pro- and eukaryotic non-neuronal cells. Thus, ACh has been detected in bacteria, algae, protozoa, tubellariae and primitive plants, suggesting an extremely early appearance of ACh in the evolutionary process.2. In humans, ACh and/or the synthesizing enzyme, choline acetyltransferase, has been demonstrated in epithelial cells (airways, alimentary tract, urogenital tract, epidermis), mesothelial (pleura, pericardium) and endothelial and muscle cells. In addition, immune cells express the non-neuronal cholinergic system (i.e. the synthesis of ACh can be detected in human leucocytes (granulocytes, lymphocytes and macrophages)), as well as in rat microglia in vitro.3. The widespread expression of non-neuronal ACh is accompanied by the ubiquitous expression of cholinesterase activity, which prevents ACh from acting as a classical hormone.4. Non-neuronal ACh mediates its cellular actions in an auto- and paracrine manner via the activation of the widely expressed nicotinic and muscarinic acetylcholine receptors, which can interfere with virtually all cellular signalling pathways (ion channels and key enzymes).5. Non-neuronal ACh appears to be involved in the regulation of basic cell functions, such as mitosis, cell differentiation, organization of the cytoskeleton, cell–cell contact, secretion and absorption. Non-neuronal ACh also plays a role in the regulation of immune functions. All these qualities together may mediate the so-called ‘trophic property’ of ACh.6. Future experiments should be designed to analyse the cellular effects of ACh in greater detail. The involvement of the non-neuronal cholinergic system in the pathogenesis of chronic inflammatory diseases should be investigated to open up new therapeutic strategies.
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  • 4
    ISSN: 1432-1440
    Keywords: Motor nerve ; Intestine ; Airways ; Neuronal nicotine receptors ; Muscular nicotine receptors ; Receptor desensitization ; [3H]Acetylcholine release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of nicotine receptor agonists on the release of [3H]acetylcholine from the phrenic nerve, the small intestine and the trachea were investigated to characterize neuronal nicotine receptors within the peripheral nervous system. Contraction of the indirectly-stimulated hemidiaphragm was recorded to investigate desensitization of the postsynaptic muscular nicotine receptors. Nicotine, cytisine, 1,1-dimethyl-4-phenylpiperazinium and 2-(4-aminophenyl)-ethyl-trimethyl-ammoniumiodide caused a concentration-dependent (0.1–30 μM) increase in evoked [3H]acetylcholine release from the phrenic nerve, whereby bell-shaped concentration-response curves were obtained. The rank order of decreasing potency was: nicotine 〉 cytisine 〉 1,1-dimethyl-4-phenylpiperazinium 〉 2-(4-aminophenyl)-ethyl-trimethyl-ammoniumiodide. The presynaptic effects of nicotine depended strongly on the exposure time: facilitation occurred after a short 20 s exposure and inhibition after a 3 min exposure, whereas nicotine no longer affected evoked [3H]acetylcholine release after a 15 min exposure. Pre-exposure (40 min) of the phrenic nerve to 0.3 μM nicotine prevented any subsequent modulatory effect of a high nicotine concentration. In contrast, the contraction of the indirectly-stimulated hemidiaphragm remained unaffected in the presence of 0.3–30 μM nicotine, but a concentration of 1 mM nicotine abolished skeletal muscle contraction. Nicotine (10 μM) produced a substantial release of [3H]acetylcholine in the small intestine but not in the isolated trachea. The present experiments show presynaptic nicotine receptors at the phrenic nerve, which, under appropriate conditions, can mediate facilitation of evoked transmitter release. These neuronal receptors appear more sensitive to desensitizing conditions than the postsynaptic muscular nicotine receptors. Nicotine also mediates a transient release of acetylcholine in the myenteric plexus but not in the trachea, and as a consequence, applied nicotine preferentially activates smooth muscle activity in the intestine.
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  • 5
    ISSN: 1432-1912
    Keywords: Guinea-pig myenteric plexus ; Acetylcholine release ; Frequency dependence ; Presynaptic muscarine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effects of scopolamine on the release of 3H-acetylcholine (ACh) from the guinea-pig myenteric plexus were studied at different stimulation frequencies (0.03–10 Hz) and train lengths (1–180 pulses). Release of 3H-ACh was measured in the absence of cholinesterase inhibitors as the outflow of tritium from myenteric plexus-longitudinal muscle preparations preloaded with 3H-choline. 2. In control experiments the volley output of 3H-ACh declined with increasing train length and increasing stimulation frequency. Stimulation by one pulse produced the highest volley output. 3. Scopolamine facilitated the evoked output of 3H-ACh via blockade of presynaptic muscarine receptors. A significant increase was already observed when the preparation was stimulated with 3 pulses at 10 Hz which indicates that the inhibitory muscarinic mechanism becomes operational within 200 ms. The facilitatory effects of scopolamine depended on both train length and frequency of stimulation. Maximal increases in 3H-ACh output were seen with brief trains (3 and 6 pulses) at a high frequency (10 Hz), or with longer trains (20 and 180 pulses) at lower frequencies (0.3 and 1 Hz). 4. Scopolamine compensated for the frequencydependent decline of 3H-ACh volley output only during brief periods of stimulation (3 and 6 pulses). It is therefore concluded that the decline in volley output during the first few pulses of a train is due to the negative feedback mechanism which is activated by the transmitter released by the preceding impulses. With longer trains of stimulation the negative feedback mechanism plays only a minor role in regulating the output per pulse.
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  • 6
    ISSN: 1432-1912
    Keywords: End-plate preparation ; Whole nerve-muscle preparation ; Choline uptake ; Choline phospholipid metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A whole nerve-muscle preparation (about 160 mg) or an end-plate preparation (about 25 mg) of the rat phrenic nerve-hemidiaphragm were incubated with [3H]choline, to investigate choline uptake and choline metabolism. Choline uptake was measured from the disappearance of choline from the incubation medium during the loading period and from the retention of tritium in the tissue after the loading and washout period. Based on the results obtained with both methods the end-plate preparation takes up three times as much choline than the whole nerve-muscle preparation or a small muscle strip that was cut outside the end-plate region and had a similar size as the end-plate preparation. Choline uptake was not markedly affected by the degree of nerve activity or by a chronic denervation. However, hemicholinium-3 significantly reduced (50%) the choline uptake by the end-plate preparation. Most of the choline (70–88%) taken up was metabolized and incorporated into membrane structures. Phosphatidylcholine was the predominant metabolite in both preparations. The ratio of phosphatidylcholine/lysophosphatidylcholine in the end-plate preparation (16) was significantly lower than in the whole nerve-muscle preparation (31). This might indicate a higher metabolism of phosphatidylcholine in the end-plate preparation. It is suggested that choline uptake by the rat phrenic nerve-hemidiaphragm occurs mainly by the muscle fibres. The innervated part of the muscle fibres can accumulate more choline than the peripheral part outside the end-plate region, probably because of a very active choline phospholipid metabolism within the end-plate region.
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  • 7
    ISSN: 1432-1912
    Keywords: Guinea-pig ileum ; Release of [3H]acetylcholine ; Autoreceptors ; Heteroreceptors ; Intraneuronal availability of calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The inhibition by three modulators (oxotremorine, noradrenaline, morphine) of acetylcholine release from the myenteric plexus preincubated with [3H]choline was investigated at different stimulation frequencies and calcium concentrations. Moreover, [3H]acetylcholine release evoked by a low (0.1 Hz) or a high (10 Hz) stimulation rate was investigated at different calcium concentrations either in the absence or presence of scopolamine. A reduced calcium concentration (0.6 mmol/l) inhibited acetylcholine release more at 0.1 Hz (74% ± 3%) than at 10 Hz (44% ± 8%). Scopolamine enhanced the stimulated acetylcholine release at a calcium concentration of 1.8 mmol/l. At calcium concentrations higher than 1.8 mmol/l scopolamine failed to enhance transmitter release markedly. A reduction of the calcium concentration (〈 1.8 mmol/l) significantly enhanced the effect of scopolamine, when acetylcholine release was evoked at 0.1 Hz. Oxotremorine (10 μmol/l) completely suppressed acetylcholine release at 1 Hz (120 pulses). When 120 pulses were applied at 10 Hz the maximal effect was only a 64% inhibition and the concentration-response curve was significantly shifted to the right. However, after a reduction of both the train length or the calcium concentration oxotremorine produced a complete inhibition of acetylcholine release evoked at 10 Hz. In contrast to the effect of oxotremorine, the concentration-response curves for morphine and noradrenaline were similar at 1 Hz and 10 Hz. Following conclusions can be drawn: 1. The present findings fit into the concept that residual calcium accumulates in the nerve terminal during 10 Hz stimulation. 2. The results obtained with scopolamine and oxotremorine are consistent with the view that muscarine autoreceptor activation triggers a reduction of the intraneuronal availability of calcium for the stimulus-secretion coupling. 3. The presynaptic effect of morphine and partly that of noradrenaline might be mediated by a different mechanism, probably by a reduction of release sites.
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  • 8
    ISSN: 1432-1912
    Keywords: Motor nerve ; [3H]Acetylcholine release ; Negative muscarinic feedback ; Positive muscarinic feedback
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neuronal transmitter stores of the rat phrenic nerve were labelled by incubation with [3H]choline. Release of [3H]acetylcholine was elicited by electrical nerve stimulation (100 or 1500 pulses, 5 or 25 Hz) or by high potassium (27 mmol/l) and the effects of the muscarine receptor agonist oxotremorine and the antagonist scopolamine were investigated. Neither oxotremorine nor scopolamine affected the basal tritium efflux. A low concentration of oxotremorine (10 nmol/l) enhanced and a high concentration of oxotremorine (1 μol/l) reduced the electrically evoked [3H]acetylcholine release. Likewise, the high potassium-evoked [3H]acetylcholine release was reduced by a high concentration of oxotremorine. Both effects of oxotremorine, increase and decrease, were abolished by a pretreatment (30 min before the first stimulation period) with 0.1 μmol/l scopolamine. Scopolamine (0.1 μol/l) alone, enhanced [3H]acetylcholine release evoked by 100 pulses (5 Hz) or by high potassium. Scopolamine, however, reduced [3H]acetylcholine release evoked by 1500 pulses (5 Hz or 25 Hz). The concentration-response curves obtained for scopolamine under these latter stimulation conditions were flat-running and biphasic which might indicate the involvement of two opposite effects (increase and decrease) of scopolamine under the present stimulation conditions. Both effects of scopolamine were reduced in the presence of 10 gmol/l neostigmine. It is concluded that muscarine receptors are present within the endplate region of motor nerves. Transmitter release from motor nerves appears to be regulated by two muscarinic feedback mechanisms. The negatively operating system is activated during short stimulation periods and the positively operating system becomes additionally apparent during long stimulation periods. Blockade of cholinesterase can hide presynaptic muscarinic mechanisms on motor nerves.
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  • 9
    ISSN: 1432-1912
    Keywords: [3H]Acetylcholine release ; Neocortex ; Myenteric plexus ; Phrenic nerve ; Calcium channel antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Electrically-evoked release of [3H]acetylcholine from autonomic neurons (myenteric plexus), motoneurons (phrenic nerve) and the central nevous system (neocortex) was investigated in the presence and absence of the calcium channel antagonists ω-conotoxin GVIA, nifedipine and verapamil, whereby the same species (rat) was used in all experiments. Release of [3H]acetylcholine was measured after incubation of the tissue with [3H]choline. ω-Conotoxin GVIA markedly reduced (70%) the evoked release of [3H]acetylcholine from the myenteric plexus of the small intestine (IC50: 0.7 nmol/l) with a similar potency at 3 and 10 Hz stimulation. An increase in the extracellular calcium concentration attenuated the inhibitory effect of ω-conotoxin GVIA. Release of [3H]acetylcholine from the rat neocortex was also inhibited (90%) by ω-conotoxin GVIA, but the potency was 19-fold lower (IC50: 13 nmol/l). However, the release of [3H]acetylcholine from the phrenic nerve was not reduced by ω-conotoxin GVIA (100 nmol/l) at 1.8 mmol/l calcium (normal concentration), whereas ω-conotoxin GVIA inhibited evoked [3H]acetylcholine release by 47% at 0.9 mmol/l calcium. Neither nifedipine (0.1 and 1 μmol/l) nor verapamil (0.1, 1 and 10 μmol/l) modified the evoked release of [3H]acetylcholine from the myenteric plexus and the phrenic nerve. Acetylcholine release from different neurons appears to be regulated by different types of calcium channels. N-type channels play the dominant role in regulating acetylcholine release from both the myenteric plexus and the neocortex, whereas acetylcholine release from motor nerves is regulated by calcium channel(s) not yet characterized.
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  • 10
    ISSN: 1432-1912
    Keywords: Isolated trachea ; [3H]Acetylcholine-release ; Epithelium-derived inhibition ; Reverse phase HPLC ; Indomethacin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate presynaptic, regulatory mechanisms on parasympathetic nerve fibres innervating the airways, the release of newly-synthesized [3H]acetylcholine from the isolated trachea was studied. Reverse phase HPLC followed by liquid scintillation spectrometry was used to separate and quantify the radioactive compounds choline, phosphorylcholine and acetylcholine in the incubation medium and the tissue. During the incubation of the tracheae with [3H]choline a significant synthesis of [3H]acetylcholine (35,000 dpm/preparation) and [3H]phosphorylcholine (500,000 dpm/preparation) occurred. In epithelium-deficient tracheae the formation of [3H]phosphorylcholine was enhanced, whereas the content of [3H]acetylcholine remained unchanged. The spontaneous outflow of tritium consisted mainly of [3H]phosphorylcholine (900 dpm/3 min) and [3H]choline (800 dpm/3 min); [3H]acetylcholine was only a minor fraction (50 dpm/3 min). Electrical stimulation of tracheae with intact epithelium caused only a small release of [3H]acetylcholine (460 dpm in the sample obtained during stimulation), but a considerable outflow of [3H]phosphorylcholine (1,900 dpm) without affecting the outflow of [3H]choline. Electrical stimulation of epithelium-deficient tracheae, however, induced a substantial release of [3H]acetylcholine (2,400 dpm), but only a small outflow of [3H]phosphorylcholine. Chemical stimulation (30 μmol/1 veratridine) also caused a large release of [3H]acetylcholine (1,700 dpm) without affecting the outflow of [3H]phosphorylcholine or [3H]choline. Indomethacin (3 μmol/1) enhanced the electrically-evoked release of [3H]acetylcholine from tracheae with intact epithelium by 89%. The present experiments demonstrate a strong inhibition by the epithelium of the electrically-evoked release of [3H]acetylcholine from the isolated guinea-pig trachea. Cyclooxygenase products of arachidonic acid do not appear as the main mediators of the epithelium-derived inhibition of acetylcholine release.
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