M Schemann

Technische Universität München, München, Bavaria, Germany

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Publications (213)905.54 Total impact

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    ABSTRACT: Innervation interacts with enteric immune responses. Chronic intestinal inflammation is associated with increased risk of colorectal cancer. We aimed to study potential extrinsic neuronal modulation of intestinal tumor development in a mouse model. Experiments were performed with male Apc(Min/+) or wild type mice (4 weeks old, body weight approximately 20 g). Subgroups with subdiaphragmatic vagotomy (apcV/wtV), sympathetic denervation of the small intestine (apcS/wtS) or sham operated controls (apcC/wtC) were investigated (n = 6-14 per group). Three months after surgical manipulation, 10 cm of terminal ileum were excised, fixed for 48 h in 4% paraformaldehyde and all tumors were counted and their area determined in mm(2) (mean ± standard error of the mean (SEM)). Whole mounts of the muscularis of terminal ileum and duodenum (internal positive control) were also stained for tyrosine hydroxylase to confirm successful sympathetic denervation. Tumor count in Apc(Min/+) mice was 62 ± 8 (apcC), 46 ± 11 (apcV) and 54 ± 8 (apcS) which was increased compared to wildtype controls with 4 ± 0.5 (wtC), 5 ± 0.5 (wtV) and 5 ± 0.6 (wtS; all p < 0.05). For Apc(Min/+) groups, vagotomized animals showed a trend towards decreased tumor counts compared to sham operated Apc(Min/+) controls while sympathetic denervation was similar to sham Apc(Min/+). Area covered by tumors in Apc(Min/+) mice was 55 ± 10 (apcC), 31 ± 8 (apcV) and 42 ± 8 (apcS) mm(2), which was generally increased compared to wildtype controls with 7 ± 0.6 (wtC), 7 ± 0.4 (wtV) and 7 ± 0.6 (wtS) mm(2) (all p < 0.05). In Apc(Min/+) groups, tumor area was decreased in vagotomized animals compared to sham operated controls (p < 0.05) while sympathetically denervated mice showed a minor trend to decreased tumor area compared to controls. Extrinsic innervation of the small bowel is likely to modulate tumor development in Apc(Min/+) mice. Interrupted vagal innervation, but not sympathetic denervation, seems to inhibit tumor growth.
    Journal of Experimental & Clinical Cancer Research 04/2015; 34(1):39. DOI:10.1186/s13046-015-0159-0 · 3.27 Impact Factor
  • Gastroenterology 04/2015; 148(4):S-131. DOI:10.1016/S0016-5085(15)30454-6 · 13.93 Impact Factor
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    ABSTRACT: The role of purinergic signaling in the human ENS is not well understood. We sought to further characterize the neuropharmacology of purinergic receptors in human ENS and test the hypothesis that endogenous purines are critical regulators of neurotransmission. LSCM-Fluo-4-(Ca(2+))-imaging of postsynaptic Ca(2+) transients (PSCaTs) was used as a reporter of neural activity. Synaptic transmission was evoked by fiber tract electrical stimulation in human SMP surgical preparations. Pharmacological analysis of purinergic signaling was done in 1,520 neurons from 241 separate ganglia, 104 patients; immunochemical labeling for P2XRs of neurons in ganglia from 19 patients. Real-time MSORT (Di-8-ANEPPS) imaging was used to test effects of adenosine on fast excitatory synaptic potentials (fEPSPs). Synaptic transmission is sensitive to pharmacological manipulations that alter accumulation of extracellular purines. Apyrase blocks PSCaTs in a majority of neurons. An ecto-NTPDase-inhibitor 6-N,N-diethyl-D-β,γ-dibromomethyleneATP or adenosine deaminase augments PSCaTs. Blockade of reuptake/deamination of eADO inhibits PSCaTs. Adenosine inhibits fEPSPs and PSCaTs (IC50=25μM), sensitive to MRS1220-antagonism (A3AR). A P2Y agonist ADPβS inhibits PSCaTs (IC50=111nM) in neurons without stimulatory ADPβS responses (EC50=960nM). ATP or a P2X1,2,2/3 (α,β-MeATP) agonist evokes fast, slow, biphasic Ca(2+) transients or Ca(2+) oscillations (EC50=400μM). PSCaTs are sensitive to P2X1 antagonist NF279. Low (20nM) or high (5μM) concentrations of P2X antagonist TNP-ATP block PSCaTs in different neurons; proportions of neurons with P2XR-ir follow the order P2X2>P2X1>P2X3; P2X1+ P2X2 and P2X3+P2X2 are co-localized. RT-PCR identified mRNA-transcripts for P2X1-7,P2Y1,2,12-14R. Responsive neurons were also identified by HuC/D-ir. Purines are critical regulators of neurotransmission in the human enteric nervous system. Purinergic signaling involves P2X1, P2X2, P2X3 channels, P2X1+P2X2 co-localization and inhibitory P2Y or A3 receptors. These are potential novel therapeutic targets for neurogastroenterology. Published by Elsevier Ltd.
    Neuropharmacology 02/2015; 95. DOI:10.1016/j.neuropharm.2015.02.014 · 4.82 Impact Factor
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    ABSTRACT: Based on the discomfort/pain threshold during rectal distension, Irritable Bowel Syndrome (IBS) patients may be subtyped as normo- or hypersensitive. We previously showed that mucosal biopsy supernatants from IBS patients activated enteric and visceral afferent neurons. We tested the hypothesis that visceral sensitivity is linked to the degree of neuronal activation. Normo- and hypersensitive IBS patients were distinguished by their discomfort/pain threshold to rectal balloon distension with a barostat. Using potentiometric and Ca(2+) dye imaging, we recorded the response of guinea pig enteric submucous and mouse dorsal root ganglion (DRG) neurons, respectively, to mucosal biopsy supernatants from normosensitive (n = 12 tested in enteric neurons, n = 9 tested in DRG) and hypersensitive IBS (n = 9, tested in both types of neurons) patients. In addition, we analyzed the association between neuronal activation and individual discomfort/pain pressure thresholds. IBS supernatants evoked Ca(2+) transients in DRG neurons and spike discharge in submucous neurons. Submucous and DRG neurons showed significantly stronger responses to supernatants from hypersensitive IBS patients as reflected by higher spike frequency or stronger [Ca(2+)]i transients in a larger proportion of neurons. The neuroindex as a product of spike frequency or [Ca(2+)]i transients and proportion of responding neurons significantly correlated with the individual discomfort/pain thresholds of the IBS patients. Supernatants from hypersensitive IBS patients caused stronger activation of enteric and DRG neurons. The level of activation correlated with the individual discomfort/pain threshold pressure values. These findings support our hypothesis that visceral sensitivity is linked to activation of peripheral neurons by biopsy supernatants. This article is protected by copyright. All rights reserved.
    Experimental physiology 06/2014; 99(10). DOI:10.1113/expphysiol.2014.080036 · 2.87 Impact Factor
  • Michel Neunlist, Michael Schemann
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    ABSTRACT: The enteric nervous system (ENS) integrates numerous sensory signals in order to control and maintain normal gut functions. Nutrients are one of the prominent factors which determine the chemical milieu in the lumen and, after absorption, also within the gut wall. This topical review summarizes current knowledge on the impact of key nutrients on ENS functions and phenotype, covering their acute and long-term effects. Enteric neurones contain the molecular machinery to respond specifically to nutrients. These transporters and receptors are not expressed exclusively in the ENS but are also present in other cells such as enteroendocrine cells (EEC) and extrinsic sensory nerves, signalling satiety or hunger. Glucose, amino acids and fatty acids all activate enteric neurones, as suggested by enhanced c-Fos expression or spike discharge. These excitatory effects are the result of a direct neuronal activation but also involve activation of EEC which, upon activation by luminal nutrients, release mediators such as ghrelin, cholecystokinin or serotonin. The presence or absence of nutrients in the intestinal lumen induces long-term changes in neurotransmitter expression, excitability, neuronal survival and ultimately impact upon gut motility, secretion or intestinal permeability. Together with EEC and vagal nerves, the ENS must be recognized as an important player initiating concerted responses to nutrients. It remains to be studied how, for instance, nutrient-induced changes in the ENS may influence additional gut functions such as intestinal barrier repair, intestinal epithelial stem cell proliferation/differentiation and also the signalling of extrinsic nerves to brain regions which control food intake. This article is protected by copyright. All rights reserved.
    The Journal of Physiology 06/2014; 592(14). DOI:10.1113/jphysiol.2014.272948 · 4.54 Impact Factor
  • Gastroenterology 05/2014; 146(5):S-82-S-83. DOI:10.1016/S0016-5085(14)60296-1 · 13.93 Impact Factor
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    ABSTRACT: Although animal models of the irritable bowel syndrome (IBS) have provided important insights, there are no models that fully express the features of this complex condition. One alternative approach is the use of human intestinal biopsies obtained during endoscopic procedures to examine peripheral mechanisms in this disorder. These studies have served to confirm the existence of peripheral pathways in humans with IBS and have provided many new mechanistic insights. Two general approaches have been employed; one approach has been to examine the biological activity of mediators within the mucosal tissue of IBS patients and the other has been to examine changes in the structural properties of key signaling pathways contained within the biopsies. Using these approaches, important changes have been discovered involving the enteric nervous system and the extrinsic sensory pathway (dorsal root ganglia neurons), the immune system, and epithelial signaling in IBS patients compared to healthy subjects. This review will systematically explore these mechanistic pathways, highlight the implications of these novel findings and discuss some of the important limitations of this approach.
    Neurogastroenterology and Motility 02/2014; DOI:10.1111/nmo.12316 · 3.42 Impact Factor
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    ABSTRACT: OBJECTIVES:Abnormal pain perception or visceral hypersensitivity (VH) is considered to be an important mechanism underlying symptoms in a subgroup of irritable bowel syndrome (IBS) patients. Increased TRPV1 (transient receptor potential cation channel subfamily V member 1) expression in rectal biopsies of IBS patients suggests a potentially important role for this nociceptor in the pathophysiology of IBS. However, evidence underscoring the involvement of TRPV1 in visceral perception in IBS is lacking. The objective of this study was to evaluate the role of TRPV1 in VH to rectal distension and clinical symptoms in patients with IBS.METHODS:A total of 48 IBS patients and 25 healthy volunteers (HVs) were invited to undergo subsequent assessment of sensitivity to rectal distensions and rectal capsaicin applications. Visceral sensitivity was evaluated by rectal distension at 3, 9, and 21 mm Hg above minimal distension pressure (MDP). Capsaicin was applied to the rectal mucosa (0.01%, 0.1%, or solvent only in random order). Visceral sensations (urge to defecate, pain, burning, and warmth sensation) were scored on a 100-mm visual analog scale (VAS). TRPV1 expression in rectal biopsies was determined by immunohistochemistry and real-time PCR.RESULTS:A total of 23 IBS patients (48%) were hypersensitive to rectal distensions (VH-IBS). A concentration-dependent increase of urge and pain perception was present in HVs and IBS patients during capsaicin 0.01 and 0.1% applications. VH-IBS patients experienced a significantly increased perception of pain, but not urge, during capsaicin applications compared with normosensitive patients (ns-IBS) and HVs. Increased pain perception was significantly associated with anxiety and VH, symptoms scores of abdominal pain, loose stools, and stool frequency. Anxiety experienced during the experimental procedure was enhanced in VH-IBS patients but not in ns-IBS or HVs. However, rectal TRPV1 expression was similar in VH-IBS, ns-IBS, and HVs on both mRNA and protein expression levels. TRPV1 expression levels did not correlate with pain perception to capsaicin or clinical symptoms in IBS patients or the subgroups.CONCLUSIONS:IBS patients with VH to rectal distension reveal increased pain perception to rectal application of capsaicin, as well as an increased anxiety response. No evidence for TRPV1 upregulation could be demonstrated. As both VH and anxiety are independently associated with increased pain perception to rectal capsaicin application, our data suggest that both peripheral and central factors are involved, with increased receptor sensitivity as a speculative possibility.Am J Gastroenterol advance online publication, 5 November 2013; doi:10.1038/ajg.2013.371.
    The American Journal of Gastroenterology 11/2013; 109(1). DOI:10.1038/ajg.2013.371 · 9.21 Impact Factor
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    ABSTRACT: The cholinergic anti-inflammatory pathway is an endogenous mechanism by which the autonomic nervous system attenuates macrophage activation via nicotinic acetylcholine receptors (nAChR). This concept has however not been demonstrated at a cellular level in intact tissue. To this end, we have studied the effect of nicotine on the activation of resident macrophages in a mouse stomach preparation by means of calcium imaging. Calcium transients ([Ca(2+)]i) in resident macrophages were recorded in a mouse stomach preparation containing myenteric plexus and muscle layers by Fluo-4. Activation of macrophages was achieved by focal puff administration of ATP. The effects of nicotine on activation of macrophages were evaluated and the nAChR involved was pharmacologically characterized. The proximity of cholinergic nerves to macrophages was quantified by confocal microscopy. Expression of β2 and α7 nAChR was evaluated by β2 immunohistochemistry and fluorophore-tagged α-bungarotoxin. In 83% of macrophages cholinergic varicose nerve fibers were detected at distances <900nm. The ATP induced [Ca(2+)]i increase was significantly inhibited in 65% or 55% of macrophages by 100µM or 10µM nicotine, respectively. This inhibitory effect was reversed by the β2 nAChR preferring antagonist dihydro-β-eryhtroidine but not by hexamethonium (non-selective nAChR-antagonist), mecamylamine (α3β4 nAChR-preferring antagonist), α-bungarotoxin or methyllycaconitine (both α7 nAChR-preferring antagonist). Macrophages in the stomach express β2 but not α7 nAChR at protein level, while those in the intestine express both receptor subunits. This study is the first in situ demonstration of an inhibition of macrophage activation by nicotine suggesting functional signaling between cholinergic neurons and macrophages in the stomach. The data suggest that the β2 subunit of the nAChR is critically involved in the nicotine-induced inhibition of these resident macrophages.
    PLoS ONE 11/2013; 8(11):e79264. DOI:10.1371/journal.pone.0079264 · 3.53 Impact Factor
  • T. Frieling, M. Schemann
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    ABSTRACT: Das Reizdarmsyndrom (RDS) ist einer der häufigsten Gründe, warum Patienten den Arzt aufsuchen, und stellt hierdurch eine erhebliche sozioökonomische Belastung dar. Das RDS wurde aufgrund der geschichtlichen Entwicklung bisher symptomenbasiert definiert. Diese symptomenbasierte Definition durch Symptomencluster als Krankheit ist problematisch, da sich das hierdurch definierte Patientenkollektiv bezüglich des Krankheitsverlaufs nicht grundsätzlich von anderen Erkrankungen unterscheidet. Neuere Untersuchungen zeigen, dass das RDS mit verschiedenen strukturellen, molekularen, genetischen, immunologischen, nervalen und psychosozialen Veränderungen assoziiert ist. Die vielen heute diskutierten Pathomechanismen spiegeln zum einen den multifaktoriellen Charakter des RDS wider, sind zum anderen aber auch Hinweise auf pathophysiologisch unterschiedliche Erkrankungen. Es ist zu erwarten, dass in Zukunft die weitere Aufklärung pathophysiologisch relevanter Faktoren und insbesondere deren Korrelation mit den klinischen Symptomen die Diagnostik und Therapie des Reizdarmsyndroms verbessert. Es wird ein wesentliches Ziel sein, Biomarker zur Charakterisierung der zahlreichen RDS-Untergruppen zu finden, damit eine spezifische Therapieentscheidung möglich ist.
    Der Gastroenterologe 09/2013; 8(5). DOI:10.1007/s11377-013-0782-2
  • 08/2013; 14(Suppl 1):O30-O30. DOI:10.1186/2050-6511-14-S1-O30
  • 08/2013; 14(Suppl 1):P34-P34. DOI:10.1186/2050-6511-14-S1-P34
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    ABSTRACT: Colonic transit and mucosal integrity are believed to be impaired in obesity. However, a comprehensive assessment of altered colonic functions, inflammatory changes and neuronal signalling of obese animals is missing. We studied in mice the impact of diet induced obesity (DIO) on: i) in vivo colonic transit; ii) signalling in the myenteric plexus by recording responses to nicotine and 2-methyl-5-HT together with the expression of tryptophan hydroxylase (TPH) 1 and 2, serotonin reuptake transporter, choline acetyltransferase and the paired box gene 4; iii) expression of proinflammatory cytokines, epithelial permeability and density of macrophages, mast cells and enterochromaffin (EC) cells. Compared to controls, colon transit and neuronal sensitivity to nicotine and 2-methyl-5-HT were enhanced in DIO mice fed for 12 weeks. This was associated with increased tissue acetylcholine and 5-HT content, and increased expressions of TPH1 and TPH2. In DIO mice, upregulation of proinflammatory cytokines was found in fat tissue but not in the gut wall. Accordingly, mucosal permeability or integrity was unaltered without signs of immune cell infiltration in the gut wall. Body weight showed positive correlations with adipocyte markers, tissue levels of 5-HT and acetylcholine and the degree of neuronal sensitization. DIO mice fed for 4 weeks showed no neuronal sensitization, had no signs of gut wall inflammation and a smaller increase in leptin, IL-6 and MCP1 expression in fat tissue. DIO is associated with faster colonic transit and impacts on acetylcholine and 5-HT metabolisms with enhanced responsiveness of enteric neurons to both mediators after 12 weeks feeding. Our study demonstrates neuronal plasticity in DIO prior to the development of a pathological histology or abnormal mucosal functions. This questions the common assumption that increased mucosal inflammation and permeability initiate functional disorders in obesity.
    The Journal of Physiology 08/2013; 591(20). DOI:10.1113/jphysiol.2013.262733 · 4.54 Impact Factor
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    ABSTRACT: The cholinergic anti-inflammatory pathway (CAIP) has been proposed as a key mechanism by which the brain, through the vagus nerve, modulates the immune system in the spleen. Vagus nerve stimulation (VNS) reduces intestinal inflammation and improves postoperative ileus. We investigated the neural pathway involved and the cells mediating the anti-inflammatory effect of VNS in the gut. The effect of VNS on intestinal inflammation and transit was investigated in wild-type, splenic denervated and Rag-1 knockout mice. To define the possible role of α7 nicotinic acetylcholine receptor (α7nAChR), we used knockout and bone marrow chimaera mice. Anterograde tracing of vagal efferents, cell sorting and Ca(2+) imaging were used to reveal the intestinal cells targeted by the vagus nerve. VNS attenuates surgery-induced intestinal inflammation and improves postoperative intestinal transit in wild-type, splenic denervated and T-cell-deficient mice. In contrast, VNS is ineffective in α7nAChR knockout mice and α7nAChR-deficient bone marrow chimaera mice. Anterograde labelling fails to detect vagal efferents contacting resident macrophages, but shows close contacts between cholinergic myenteric neurons and resident macrophages expressing α7nAChR. Finally, α7nAChR activation modulates ATP-induced Ca(2+) response in small intestine resident macrophages. We show that the anti-inflammatory effect of the VNS in the intestine is independent of the spleen and T cells. Instead, the vagus nerve interacts with cholinergic myenteric neurons in close contact with the muscularis macrophages. Our data suggest that intestinal muscularis resident macrophages expressing α7nAChR are most likely the ultimate target of the gastrointestinal CAIP.
    Gut 08/2013; 63(6). DOI:10.1136/gutjnl-2013-304676 · 13.32 Impact Factor
  • Autonomic Neuroscience 08/2013; 177(1). DOI:10.1016/j.autneu.2013.05.042 · 1.37 Impact Factor
  • Zeitschrift für Gastroenterologie 07/2013; 51(7):651-72. DOI:10.1055/s-0033-1335808 · 1.67 Impact Factor
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    ABSTRACT: BACKGROUND: Hyoscine butylbromide (HBB, Buscopan(®) ) is clinically used to treat intestinal cramps and visceral pain. Various studies, mainly on animal tissues, suggested that its antimuscarinic action is responsible for its spasmolytic effect. However, functional in vitro studies with human tissue have not been performed so far. METHODS: We wanted to provide a comprehensive study on the mode of action of HBB in human intestinal samples and investigated HBB (1 nmol L(-1) -10 μmol L(-1) ) effects on muscle activity with isometric force transducers and calcium imaging, on epithelial secretion with Ussing chamber technique and on enteric neurons using fast neuroimaging. KEY RESULTS: Hyoscine butylbromide concentration dependently reduced muscle contractions, calcium mobilization, and epithelial secretion induced by the muscarinic agonist bethanechol with IC50 values of 429, 121, and 224 nmol L(-1) , respectively. Forskolin-induced secretion was not altered by HBB. Cholinergic muscarinic muscle and epithelial responses evoked by electrical nerve stimulation were inhibited by 1-10 μmol L(-1) HBB. Moreover, HBB significantly reduced the bethanechol-induced action potential discharge in enteric neurons. Interestingly, we observed that high concentrations of HBB (10 μmol L(-1) ) moderately decreased nicotinic receptor-mediated secretion, motility, and nerve activity. CONCLUSIONS & INFERENCES: The results demonstrated the strong antimuscarinic action of HBB whereas the nicotinic antagonism at higher concentrations plays at most a moderate modulatory role. The muscle relaxing effect of HBB and its inhibition of muscarinic nerve activation likely explain its clinical use as an antispasmodic drug. Our results further highlight a so far unknown antisecretory action of HBB which warrants further clinical studies on its use in secretory disorders.
    Neurogastroenterology and Motility 05/2013; 25(8). DOI:10.1111/nmo.12156 · 3.42 Impact Factor
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    ABSTRACT: The enteric nervous system contains excitatory and inhibitory neurons, which control contraction and relaxation of smooth muscle cells as well as gastrointestinal motor activity. Little is known about the exact cellular mechanisms of neuronal signal transduction to smooth muscle cells in the gut. Here we generate a c-Kit(CreERT2) knock-in allele to target a distinct population of pacemaker cells called interstitial cells of Cajal. By genetic loss-of-function studies, we show that interstitial cells of Cajal, which generate spontaneous electrical slow waves and thus rhythmic contractions of the smooth musculature, are essential for transmission of signals from enteric neurons to gastrointestinal smooth muscle cells. Interstitial cells of Cajal, therefore, integrate excitatory and inhibitory neurotransmission with slow-wave activity to orchestrate peristaltic motor activity of the gut. Impairment of the function of interstitial cells of Cajal causes severe gastrointestinal motor disorders. The results of our study show at the genetic level that these disorders are not only due to loss of slow-wave activity but also due to disturbed neurotransmission.
    Nature Communications 03/2013; 4:1630. DOI:10.1038/ncomms2626 · 10.74 Impact Factor
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    ABSTRACT: BACKGROUND: Beneficial effects of ginger in the treatment of gastrointestinal (GI) problems and chemotherapy-induced nausea and vomiting are well accepted. In rodents, the action of ginger seems to be mediated by the inhibition of 5-HT3 receptors, which are established targets to combat emesis and irritable bowel syndrome. METHODS: Heterologously expressed human 5-HT3 A or 5-HT3 AB receptors were characterized by means of Ca(2+) influx studies using HEK293 cells. Complementing Ca(2+) measurements in Fluo-4-AM-stained whole-mount preparations of the human submucous plexus were carried out. Furthermore, [3H]GR65630 binding assays were performed to reveal the mode of action of ginger and its pungent compounds. KEY RESULTS: We show for the first time that ginger extracts and its pungent arylalkane constituents concentration-dependently inhibit activation of human 5-HT3 receptors. Ginger extracts inhibited both receptors with increasing content of pungent compounds, confirming that these are part of ginger's active principle. Inhibition potencies of the arylalkanes 6-gingerol and 6-shogaol on both receptors were in the low micromolar range. A lipophilic ginger extract and 6-gingerol had no influence on 5-HT potency, but reduced the 5-HT maximum effect, indicating non-competitive inhibition. The non-competitive action was confirmed by [(3) H]GR65630 binding, showing that the ginger extract did not displace the radioligand from 5-HT3 A and 5-HT3 AB receptors. The potential relevance of the inhibitory action of ginger on native 5-HT3 receptors in the gut was confirmed in whole-mount preparations of the human submucous plexus. While a general neurotoxic effect of 6-gingerol was ruled out, it inhibited the 2-methyl-5-HT-mediated activation of 5-HT3 receptors residing on enteric neurons. CONCLUSIONS & INFERENCES: Our findings may encourage the use of ginger extracts to alleviate nausea in cancer patients receiving chemotherapy and to treat functional GI disorders.
    Neurogastroenterology and Motility 03/2013; 25(5). DOI:10.1111/nmo.12107 · 3.42 Impact Factor
  • Zeitschrift für Phytotherapie 03/2013; 34(S 01). DOI:10.1055/s-0033-1338228

Publication Stats

4k Citations
905.54 Total Impact Points


  • 2003–2015
    • Technische Universität München
      • Chair of Human Biology
      München, Bavaria, Germany
  • 2013
    • Catholic University of Louvain
      Лувен-ла-Нев, Walloon, Belgium
  • 2009
    • University of Bristol
      Bristol, England, United Kingdom
  • 1995–2007
    • The University of Sheffield
      • Department of Biomedical Science
      Sheffield, ENG, United Kingdom
    • Bulgarian Academy of Sciences
      Ulpia Serdica, Sofia-Capital, Bulgaria
  • 1995–2002
    • University of Veterinary Medicine Hannover
      • Institute of Physiology
      Hanover, Lower Saxony, Germany
  • 2000
    • Heinrich-Heine-Universität Düsseldorf
      • Klinik für Gastroenterologie, Hepatologie und Infektiologie
      Düsseldorf, North Rhine-Westphalia, Germany
  • 1999
    • Hannover Medical School
      Hanover, Lower Saxony, Germany
  • 1995–1999
    • Hochschule Hannover
      Hanover, Lower Saxony, Germany
  • 1993
    • Tokai University
      • School of Medicine
      Hiratsuka, Kanagawa-ken, Japan
  • 1985–1992
    • Hohenheim University
      • Institute of Physiology
      Stuttgart, Baden-Württemberg, Germany
  • 1989
    • The Ohio State University
      • Department of Physiology and Cell Biology
      Columbus, Ohio, United States