The role of endogenous cholecystokinin in the sensory transduction of luminal nutrient signals in the rat jejunum

Eastwood, C.; Maubach, Karen A.; Kirkup, Anthony J.; Grundy, David

doi:10.1016/s0304-3940(98)00666-1

Cited by 86 publications

(49 citation statements)

References 7 publications

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“…Similar transduction for mucosal chemosensory afferents can range from a few hundred ms for acetate 33 to 10 or 20 s for amino acids 37,38 , long-chain fatty acids 39 or glucose 35 . As responses to JB-1 were about 8 s, it is unlikely that it's inter-kingdom signalling molecule is acetate or low pH but would be consistent with a saccharide, as we have shown for PSA.…”

Section: Discussionmentioning

confidence: 99%

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

et al. 2013

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Symbionts or probiotics are known to affect the nervous system. To understand the mechanisms involved, it is important to measure sensory neuron responses and identify molecules responsible for this interaction. Here we test the effects of adding Lactobacillus rhamnosus (JB-1) and Bacteroides fragilis to the epithelium while making voltage recordings from intestinal primary afferent neurons. Sensory responses are recorded within 8 s of applying JB-1 and excitability facilitated within 15 min. Bacteroides fragilis produces similar results, as does its isolated, capsular exopolysaccharide, polysaccharide A. Lipopolysaccharide-free polysaccharide A completely mimics the neuronal effects of the parent organism. Experiments with a mutant Bacteroides fragilis devoid of polysaccharide A shows that polysaccharide A is necessary and sufficient for the neuronal effects. Complex carbohydrates have not been reported before as candidates for such signalling between symbionts and the host. These observations indicate new neuronal targets and invite further study of bacterial carbohydrates as inter-kingdom signalling molecules between beneficial bacteria and sensory neurons.

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Section: Discussionmentioning

confidence: 99%

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

et al. 2013

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“…Interestingly, however, as mentioned previously, application of DB to GI cells stimulates the release of CCK (8,18). While CCK is generally considered a satiety hormone that exerts its effects through both vagal and nonvagal (humoral) routes at various peripheral and central targets (3,27,34), it is also believed to convey stimulusspecific information in a paracrine fashion at local sensory afferent terminals (15,36). If CCK is involved as a critical chemosensory signaling component, then pretreatment with devazepide, a CCK-1R antagonist, should abolish the early response to intraduodenal DB, compared with pretreatment with its vehicle.…”

Section: Experiments 1: Rats Rapidly Suppress Ongoing Intake In Re-mentioning

confidence: 94%

Ongoing ingestive behavior is rapidly suppressed by a preabsorptive, intestinal “bitter taste” cue

Schier

Davidson

Powley

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Schier LA, Davidson TL, Powley TL. Ongoing ingestive behavior is rapidly suppressed by a preabsorptive, intestinal "bitter taste" cue. Am J Physiol Regul Integr Comp Physiol 301: R1557-R1568, 2011. First published August 24, 2011 doi:10.1152/ajpregu.00344.2011.-The discovery that cells in the gastrointestinal (GI) tract express the same molecular receptors and intracellular signaling components known to be involved in taste has generated great interest in potential functions of such post-oral "taste" receptors in the control of food intake. To determine whether taste cues in the GI tract are detected and can directly influence behavior, the present study used a microbehavioral analysis of intake, in which rats drank from lickometers that were programmed to simultaneously deliver a brief yoked infusion of a taste stimulus to the intestines. Specifically, in daily 30-min sessions, thirsty rats with indwelling intraduodenal catheters were trained to drink hypotonic (0.12 M) sodium chloride (NaCl) and simultaneously self-infuse a 0.12 M NaCl solution. Once trained, in a subsequent series of intestinal taste probe trials, rats reduced licking during a 6-min infusion period, when a bitter stimulus denatonium benzoate (DB; 10 mM) was added to the NaCl vehicle for infusion, apparently conditioning a mild taste aversion. Presentation of the DB in isomolar lithium chloride (LiCl) for intestinal infusions accelerated the development of the response across trials and strengthened the temporal resolution of the early licking suppression in response to the arrival of the DB in the intestine. In an experiment to evaluate whether CCK is involved as a paracrine signal in transducing the intestinal taste of DB, the CCK-1R antagonist devazepide partially blocked the response to intestinal DB. In contrast to their ability to detect and avoid the bitter taste in the intestine, rats did not modify their licking to saccharin intraduodenal probe infusions. The intestinal taste aversion paradigm developed here provides a sensitive and effective protocol for evaluating which tastants-and concentrations of tastants-in the lumen of the gut can control ingestion. chemoreceptor; gastrointestinal; denatonium benzoate; food learning; cholecystokinin CHEMORECEPTORS ARE INDISPENSABLE to the control of food intake. As taste receptors on the tongue and in the oral cavity, they supply signals critical for accepting and rejecting foods for consumption, promoting intake of palatable foods, and preparing the digestive system for the arrival of nutrients. Complementary to this early oral sensory processing, chemoreceptors in the stomach and intestines transduce signals from the lumen to adjust motility, secrete digestive enzymes, and initiate satiation (cf., 24). Accordingly, the gastrointestinal (GI) tract has been conventionally considered to have a more or less continuous sensory surface for tracking meals to engage and revise apposite and coordinated responses particular to the properties of the food and the body's physiological state. Despite th...

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“…57 CCK excites vagal afferent fibres with mucosal endings, 58 and both long chain fatty acids and casein cause activation of vagal mucosal afferents, which is blocked by CCK A antagonists. 59,60 PYY also excites vagal afferent neurons and its satiety-mediating effects might require intact vagal nerve connections, 61,62 although it also acts hormonally in the brain. 63 Even the prototypical hormone, secretin, activates a subset of vagal mucosal afferent neurons.…”

Section: Vagal Mucosal Afferentsmentioning

confidence: 99%

Extrinsic primary afferent signalling in the gut

Brookes

Spencer

Costa

et al. 2013

Nat Rev Gastroenterol Hepatol

246

216

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Visceral sensory neurons activate reflex pathways that control gut function and also give rise to important sensations, such as fullness, bloating, nausea, discomfort, urgency and pain. Sensory neurons are organised into three distinct anatomical pathways to the central nervous system (vagal, thoracolumbar and lumbosacral). Although remarkable progress has been made in characterizing the roles of many ion channels, receptors, and second messengers in visceral sensory neurons, the basic aim of understanding how many classes there are, and how they differ, has proven difficult to achieve. We suggest that there are just five structurally distinct types of sensory endings in the gut wall that account for essentially all of the primary afferent neurons in the three pathways. Each of these five major structural types of endings seems to show distinctive combinations of physiological responses. These types are: 'intraganglionic laminar' endings in myenteric ganglia; 'mucosal' endings located in the subepithelial layer; 'muscular mucosal' afferents, with mechanosensitive endings close to the muscularis mucosae; 'intramuscular' endings, with endings within the smooth muscle layers; and 'vascular' afferents, with sensitive endings primarily on blood vessels. 'Silent' afferents might be a subset of inexcitable 'vascular' afferents, which can be switched on by inflammatory mediators.Extrinsic sensory neurons comprise an attractive focus for targeted therapeutic intervention in a range of gastrointestinal disorders.2

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The role of endogenous cholecystokinin in the sensory transduction of luminal nutrient signals in the rat jejunum

Cited by 86 publications

References 7 publications

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

Bacteroides fragilis polysaccharide A is necessary and sufficient for acute activation of intestinal sensory neurons

Ongoing ingestive behavior is rapidly suppressed by a preabsorptive, intestinal “bitter taste” cue

Extrinsic primary afferent signalling in the gut

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