Retracted: Serotonin and cholecystokinin synergistically stimulate rat vagal primary afferent neurones

Li, Ying; Owyang, Chung

doi:10.1113/jphysiol.2004.064816

Cited by 38 publications

(19 citation statements)

References 38 publications

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“…In examining the effects of CCK on feeding, many have suggested that the actions of CCK are partially dependent on 5-HT 3 receptor activation (1,6,14). Furthermore, primary vagal afferent neurons are potently stimulated by endogenous 5-HT and CCK release (26,53), and a subpopulation of nodose ganglion neurons possess high-affinity CCK 1 receptors and 5-HT 3 receptors (24).…”

Section: Discussionmentioning

confidence: 99%

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An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

Sartor¹,

Shulkes²,

Verberne³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Sartor, Daniela M., Arthur Shulkes, and Anthony J. M. Verberne. An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats. Am J Physiol Regul Integr Comp Physiol 290: R625-R633, 2006. First published October 20, 2005 doi:10.1152/ajpregu.00639.2005.-Ingestion of a meal results in gastrointestinal (GI) hyperemia and is associated with systemic and paracrine release of a number of peptide hormones, including cholecystokinin (CCK) and 5-hydroxytryptamine (5-HT). Systemic administration of CCK octapeptide inhibits a subset of presympathetic neurons of the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor tone to the GI viscera. The aim of this study was to determine whether endogenous release of CCK and/or 5-HT also inhibits CCK-sensitive RVLM neurons. The effects of intraduodenal administration of the secretagogues sodium oleate (SO) and soybean trypsin inhibitor (SBTI) on circulating levels of CCK and 5-HT were examined. In separate experiments, the discharge rates of barosensitive, medullospinal, CCK-sensitive RVLM presympathetic vasomotor neurons were recorded after rapid intraduodenal infusion of SO-SBTI or water. Alternatively, animals were pretreated with the CCK 1 receptor antagonists devazepide and lorglumide or the 5-HT 3 antagonist MDL-72222 before SO-SBTI administration. Secretagogue infusion significantly increased the level of circulating CCK, but not 5-HT. SO-SBTI significantly decreased (58%) the neuronal firing rate of CCKsensitive RVLM neurons compared with water (5%). CCK 1 receptor antagonists did not reverse SO-SBTI-induced neuronal inhibition (58%), whereas the 5-HT 3 antagonist significantly attenuated the effect (22%). This study demonstrates a functional relation between a subset of RVLM presympathetic vasomotor neurons and meal-related signals arising from the GI tract. It is likely that endogenously released 5-HT acts in a paracrine fashion on GI 5-HT 3 receptors to initiate reflex inhibition of these neurons, resulting in GI vasodilatation by withdrawal of sympathetic tone. rostroventrolateral medulla; cholecystokinin; devazepide; MDL-72222; 5-hydroxytryptamine GASTROINTESTINAL HYPEREMIA is a physiological consequence of food consumption. Gastrointestinal hormones such as cholecystokinin (CCK) have been implicated in gastrointestinal vasodilatation associated with postprandial increase in splanchnic blood flow. The involvement of the sympathetic vasomotor system in this response is poorly understood. We recently suggested that food-related signals may produce gastrointestinal vasodilatation via a reflex withdrawal of sympathetic vasomotor outflow (39,45). In healthy individuals, the sympathetic nervous system compensates for postprandial splanchnic blood pooling by activating sympathetic vasoconstrictor drive to skeletal muscle resistance vessels in response to baroreceptor unloading. In patients with cardiovascular disease associated with diabetic neuropathy or autonomic dysfunction, poor baroreflex comp...

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Section: Discussionmentioning

confidence: 99%

“…It has been suggested that CCK and 5-hydroxytryptamine (5-HT) act synergistically to activate vagal afferents (24). Early in vivo studies supported a role for 5-HT in the vasodilator responses elicited by CCK, secretin, or mucosal irritation (12).…”

mentioning

confidence: 99%

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

Sartor¹,

Shulkes²,

Verberne³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Transmitters released from the enteroendocrine cells in response to various stimuli, in addition to their paracrine actions on neighboring enterocytes, activate specific receptors within the enteric nervous system (15). Importantly, enteroendocrine cell products also activate receptors at afferent terminals in vagal and spinal pathways (10).…”

mentioning

confidence: 99%

“…Particular attention has been paid to the inactivation of intestinal neuroreceptors by 5-HT produced by EC cells and by CCK produced by enteroendocrine I cells. Furthermore, recent studies have shown that these two transmitters interact in stimulation of vagal primary afferent neurons (15). The transfer of information from the gut to the central nervous system has been the subject of theme articles in this journal (10,21).…”

mentioning

confidence: 99%

Epithelial Cells and Their Neighbors. II. New perspectives on efferent signaling between brain, neuroendocrine cells, and gut epithelial cells

Flemström

Sjöblom

2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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Surface sensory enteroendocrine cells are established mucosal taste cells that monitor luminal contents and provide an important link in transfer of information from gut epithelium to the central nervous system. Recent studies now show that these cells can also mediate efferent signaling from the brain to the gut. Centrally elicited stimulation of vagal and sympathetic pathways induces release of melatonin, which acts at MT2 receptors to increase mucosal electrolyte secretion. Psychological factors as well mucosal endocrine cell hyperplasia are implicated in functional intestinal disorders. Central nervous influence on the release of transmitters from gut endocrine cells offers an exciting area of future gastrointestinal research with a clinical relevance.

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“…Similarly, 55% nodose neurones possessing high-affinity CCK-A receptors also responded to luminal perfusion of 5-HT. Interestingly, we showed that although a subthreshold dose of CCK-8 produced no measurable electrophysiological effects, it augmented the neuronal response to luminal 5-HT perfusion [118] (Fig. 3).…”

Section: Serotonin and Cholecystokinin Synergistically Stimulate Rat mentioning

confidence: 93%

Sensory Signal Transduction in the Vagal Primary Afferent Neurons

Li¹

2007

CMC

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The vagal nerve conveys primary afferent information from the intestinal mucosa to the brain stem. Activation of vagal afferent fibers results in inhibition of food intake, gastric emptying, and stimulation of pancreatic secretion. Afferents nerves terminating near to the mucosa are in a position to monitor the composition of the luminal contents. As afferents do not project directly into the lumen, their activation depends on an intermediary step, i.e. neuronal activation by a secondary substance released from within the mucosal epithelium. This review addresses the role for both cholecytokinin (CCK) and serotonin (5-HT) released from enteroendocrine cells and acting as paracrine agents on the terminals of vagal afferents in responses to a number of luminal signals. CCK acted on both high- and low-affinity CCK-A receptors present on distinct vagal primary afferent neurons. Neurons of the nodose ganglia respond to intraduodenal perfusions of maltose, glucose, and hypertonic saline. These neurons were also sensitive to exogenous luminally applied 5-HT at concentrations that mimic physiologic levels. Intravenous administration of a 5-HT3 antagonist blocked these responses suggesting that nodose neuronal responses to luminal osmolarity and to the digestion products of carbohydrates are dependent on the release of endogenous 5-HT from the mucosal enterochromaffin (EC) cells, which acts on the 5-HT3 receptors on vagal afferent fibers to stimulate vagal afferent neurons. Double-labeling studies revealed that nodose neurons responded to 5-HT-dependent luminal stimuli contain mainly glutamate and substance P. Over the past year or so it has become clear that there are multiple possible excitatory inputs to a common vagal afferent route with synergistic interactions being common. The nodose ganglion contains neurons that may possess only high- or low-affinity CCK-A receptors or 5-HT3 receptors. Some neurons that express high-affinity CCK-A receptors also express 5-HT3 receptors and (or) secretin receptors. Pre-exposure to luminal 5-HT may augment the subsequent response to a subthreshold dose of CCK. Synergistic interaction between CCK and secretin also occurs at the nodose ganglia; this is mediated by high affinity CCK-A receptor. This may explain the robust postprandial secretion of enzyme, bicarbonate, and fluid despite the modest increase in CCK after a meal. Some neurons that possess low-affinity CCK-A receptor colocalize with leptin receptors (OB-Rs). These neurons also respond to mechanical distention. Interaction between CCK-A receptor and OB-Rs in these neurons likely facilitates leptin mediation of short-term satiety.

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Retracted: Serotonin and cholecystokinin synergistically stimulate rat vagal primary afferent neurones

Cited by 38 publications

References 38 publications

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats

Epithelial Cells and Their Neighbors. II. New perspectives on efferent signaling between brain, neuroendocrine cells, and gut epithelial cells

Sensory Signal Transduction in the Vagal Primary Afferent Neurons

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