scholarly journals Divergent effects of exendin‐4 and interleukin‐6 on rat colonic secretory and contractile activity are associated with changes in regional vagal afferent signaling

2021 ◽  
Author(s):  
Rebecca O'Brien ◽  
Maria M. Buckley ◽  
Dervla O'Malley
Keyword(s):  
Interleukin 6 ◽  
Contractile Activity ◽  
Vagal Afferent ◽  
Afferent Signaling

scholarly journals Intrameal Hepatic Portal and Intraperitoneal Infusions of Glucagon-Like Peptide-1 Reduce Spontaneous Meal Size in the Rat via Different Mechanisms

Endocrinology ◽  
2008 ◽  
Vol 150 (3) ◽  
pp. 1174-1181 ◽  
Author(s):  
Elisabeth B. Rüttimann ◽  
Myrtha Arnold ◽  
Jacquelien J. Hillebrand ◽  
Nori Geary ◽  
Wolfgang Langhans
Keyword(s):  
Food Intake ◽  
Vena Cava ◽  
Meal Size ◽  
Dark Phase ◽  
Hepatic Portal Vein ◽  
Vagal Afferent ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Hepatic Portal ◽  
Afferent Signaling

Peripheral administration of glucagon-like peptide (GLP)-1 reduces food intake in animals and humans, but the sites and mechanism of this effect and its physiological significance are not yet clear. To investigate these issues, we prepared rats with chronic catheters and infused GLP-1 (0.2 ml/min; 2.5 or 5.0 min) during the first spontaneous dark-phase meals. Infusions were remotely triggered 2–3 min after meal onset. Hepatic portal vein (HPV) infusion of 1.0 or 3.0 (but not 0.33) nmol/kg GLP-1 reduced the size of the ongoing meal compared with vehicle without affecting the subsequent intermeal interval, the size of subsequent meals, or cumulative food intake. In double-cannulated rats, HPV and vena cava infusions of 1.0 nmol/kg GLP-1 reduced meal size similarly. HPV GLP-1 infusions of 1.0 nmol/kg GLP-1 also reduced meal size similarly in rats with subdiaphragmatic vagal deafferentations and in sham-operated rats. Finally, HPV and ip infusions of 10 nmol/kg GLP-1 reduced meal size similarly in sham-operated rats, but only HPV GLP-1 reduced meal size in subdiaphragmatic vagal deafferentation rats. These data indicate that peripherally infused GLP-1 acutely and specifically reduces the size of ongoing meals in rats and that the satiating effect of ip, but not iv, GLP-1 requires vagal afferent signaling. The findings suggest that iv GLP-1 infusions do not inhibit eating via hepatic portal or hepatic GLP-1 receptors but may act directly on the brain. Intrameal hepatic portal and intraperitoneal (IP) infusions of GLP-1 reduce meal size in rats, but only IP GLP-1 requires vagal afferent signaling for this effect.

scholarly journals Dietary fat sensing via fatty acid oxidation in enterocytes: possible role in the control of eating

2011 ◽  
Vol 300 (3) ◽  
pp. R554-R565 ◽  
Author(s):  
Wolfgang Langhans ◽  
Claudia Leitner ◽  
Myrtha Arnold
Keyword(s):  
Fatty Acids ◽  
Small Intestine ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Energy Homeostasis ◽  
Vagal Afferents ◽  
Acid Oxidation ◽  
Physiological Relevance ◽  
Vagal Afferent ◽  
Afferent Signaling

Various mechanisms detect the presence of dietary triacylglycerols (TAG) in the digestive tract and link TAG ingestion to the regulation of energy homeostasis. We here propose a novel sensing mechanism with the potential to encode dietary TAG-derived energy by translating enterocyte fatty acid oxidation (FAO) into vagal afferent signals controlling eating. Peripheral FAO has long been implicated in the control of eating ( 141 ). The prevailing view was that mercaptoacetate (MA) and other FAO inhibitors stimulate eating by modulating vagal afferent signaling from the liver. This concept has been challenged because hepatic parenchymal vagal afferent innervation is scarce and because experimentally induced changes in hepatic FAO often fail to affect eating. Nevertheless, intraperitoneally administered MA acts in the abdomen to stimulate eating because this effect was blocked by subdiaphragmatic vagal deafferentation ( 21 ), a surgical technique that eliminates all vagal afferents from the upper gut. These and other data support a role of the small intestine rather than the liver as a FAO sensor that can influence eating. After intrajejunal infusions, MA also stimulated eating in rats through vagal afferent signaling, and after infusion into the superior mesenteric artery, MA increased the activity of celiac vagal afferent fibers originating in the proximal small intestine. Also, pharmacological interference with TAG synthesis targeting the small intestine induced a metabolic profile indicative of increased FAO and inhibited eating in rats on a high-fat diet but not on chow. Finally, cell culture studies indicate that enterocytes oxidize fatty acids, which can be modified pharmacologically. Thus enterocytes may sense dietary TAG-derived fatty acids via FAO and influence eating through changes in intestinal vagal afferent activity. Further studies are necessary to identify the link between enterocyte FAO and vagal afferents and to examine the specificity and potential physiological relevance of such a mechanism.

II. Integration of afferent signaling from the viscera by the nodose ganglia

2003 ◽  
Vol 284 (1) ◽  
pp. G8-G14 ◽  
Author(s):  
Kirsteen N. Browning ◽  
David Mendelowitz
Keyword(s):  
Sensory Neurons ◽  
Tissue Injury ◽  
Large Body ◽  
Sensory Function ◽  
Afferent Neurons ◽  
Nodose Ganglia ◽  
Vagal Afferent ◽  
Afferent Signaling ◽  
Recent Demonstration ◽  
Stimulation Of

To understand vago-vagal reflexes, one must have an appreciation of the events surrounding the encoding, integration, and central transfer of peripheral sensations by vagal afferent neurons. A large body of work has shown that vagal afferent neurons have nonuniform properties and that distinct subpopulations of neurons exist within the nodose ganglia. These sensory neurons display a considerable degree of plasticity; electrophysiological, pharmacological, and neurochemical properties have all been shown to alter after peripheral tissue injury. The validity of claims of selective recordings from populations of neurons activated by peripheral stimuli may be diminished, however, by the recent demonstration that stimulation of a subpopulation of nodose neurons can enhance the activity of unstimulated neuronal neighbors. To better understand the neurophysiological processes occurring after vagal afferent stimulation, it is essential that the electrophysiological, pharmacological, and neurochemical properties of nodose neurons are correlated with their sensory function or, at the very least, with their specific innervation target.

Vagal Afferent Signaling and the Integration of Direct and Indirect Controls of Food Intake

2017 ◽  
pp. 229-258 ◽  
Author(s):  
Robert C. Ritter ◽  
Carlos A. Campos ◽  
Jason Nasse ◽  
James H. Peters
Keyword(s):  
Food Intake ◽  
Vagal Afferent ◽  
Afferent Signaling

Enhancement of antral contractions and vagal afferent signaling with synchronized electrical stimulation

2003 ◽  
Vol 285 (3) ◽  
pp. G577-G585 ◽  
Author(s):  
Shachar Peles ◽  
Jaime Petersen ◽  
Ricardo Aviv ◽  
Shai Policker ◽  
Ossama Abu-Hatoum ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Vagal Afferents ◽  
Mechanical Stimuli ◽  
The Central Nervous System ◽  
Rhythmic Firing ◽  
Vagal Afferent ◽  
Electrically Enhanced ◽  
Smooth Muscle Contractions ◽  
Afferent Signaling ◽  
Antral Distension

Gastric filling activates vagal afferents involved in peripheral signaling to the central nervous system (CNS) for food intake. It is not known whether these afferents linearly encode increasing contractions of the antrum during antral distension (AD). The aim of this study was to investigate effects of AD and electrically enhanced antral contractions on responses of vagal afferents innervating the antrum. Single-fiber recordings were made from the vagal afferents in anesthetized male Long-Evans rats. Antral contractions were measured with a solid-state probe placed in the antrum. A nonexcitatory electrical stimulation (NES) inducing no smooth muscle contractions was applied during the ascending phase of antral contractions to enhance subsequent antral contractions. Fifty-six fibers identified during AD (1 ml for 30 s) were studied through different types of mechanical stimuli. Under normal conditions, one group of fibers exhibited rhythmic firing in phase with antral contractions. Another group of fibers had nonrhythmic spontaneous firing. Responses of 15 fibers were tested with NES during multiple-step distension (MSD). NES produced a mean increase in antral contraction amplitude (177.1 ± 35.3%) and vagal afferent firing (21.6 ± 2.6%). Results show that both passive distension and enhanced antral contractions activate distension-sensitive vagal afferents. Responses of these fibers increase linearly to enhanced antral contraction induced by NES or MSD up to a distending volume of 0.6 ml. However, responses reached a plateau at a distending volume >0.8 ml. We concluded that enhanced contraction of the antrum can activate vagal afferents signaling to the CNS.

scholarly journals Sub‐diaphragmatic vagal nerve stimulation alleviates rodent hypertension associated with gut dysbiosis and reduced serotonergic vagal afferent signaling

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Tao Yang ◽  
Basak Donertas Ayaz ◽  
Alan Araujo ◽  
Elliott W. Dirr ◽  
David M. Baekey ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Gut Dysbiosis ◽  
Vagal Afferent ◽  
Afferent Signaling

scholarly journals Loss of neurotrophin-3 from smooth muscle disrupts vagal gastrointestinal afferent signaling and satiation

2013 ◽  
Vol 305 (11) ◽  
pp. R1307-R1322 ◽  
Author(s):  
Edward A. Fox ◽  
Jessica E. Biddinger ◽  
Zachary C. Baquet ◽  
Kevin R. Jones ◽  
Jennifer McAdams
Keyword(s):  
Smooth Muscle ◽  
Area Postrema ◽  
Microstructural Analysis ◽  
Meal Size ◽  
Vagal Afferents ◽  
Eating Rate ◽  
Daily Food ◽  
Neurotrophin 3 ◽  
Vagal Afferent ◽  
Afferent Signaling

A large proportion of vagal afferents are dependent on neurotrophin-3 (NT-3) for survival. NT-3 is expressed in developing gastrointestinal (GI) smooth muscle, a tissue densely innervated by vagal mechanoreceptors, and thus could regulate their survival. We genetically ablated NT-3 from developing GI smooth muscle and examined the pattern of loss of NT-3 expression in the GI tract and whether this loss altered vagal afferent signaling or feeding behavior. Meal-induced c-Fos activation was reduced in the solitary tract nucleus and area postrema in mice with a smooth muscle-specific NT-3 knockout ( SM-NT-3 KO) compared with controls, suggesting a decrease in vagal afferent signaling. Daily food intake and body weight of SM-NT-3 KO mice and controls were similar. Meal pattern analysis revealed that mutants, however, had increases in average and total daily meal duration compared with controls. Mutants maintained normal meal size by decreasing eating rate compared with controls. Although microstructural analysis did not reveal a decrease in the rate of decay of eating in SM-NT-3 KO mice, they ate continuously during the 30-min meal, whereas controls terminated feeding after 22 min. This led to a 74% increase in first daily meal size of SM-NT-3 KO mice compared with controls. The increases in meal duration and first meal size of SM-NT-3 KO mice are consistent with reduced satiation signaling by vagal afferents. This is the first demonstration of a role for GI NT-3 in short-term controls of feeding, most likely involving effects on development of vagal GI afferents that regulate satiation.

scholarly journals Genetic and pharmacological evidence for low-abundance TRPV3 expression in primary vagal afferent neurons

2016 ◽  
Vol 310 (9) ◽  
pp. R794-R805 ◽  
Author(s):  
Shaw-wen Wu ◽  
Jonathan E. M. Lindberg ◽  
James H. Peters
Keyword(s):  
Ion Channels ◽  
Glutamate Release ◽  
Primary Cultures ◽  
Functional Expression ◽  
Ruthenium Red ◽  
Temperature Sensitive ◽  
Afferent Neurons ◽  
Ethyl Vanillin ◽  
Vagal Afferent ◽  
Afferent Signaling

Primary vagal afferent neurons express a multitude of thermosensitive ion channels. Within this family of ion channels, the heat-sensitive capsaicin receptor (TRPV1) greatly influences vagal afferent signaling by determining the threshold for action-potential initiation at the peripheral endings, while controlling temperature-sensitive forms of glutamate release at central vagal terminals. Genetic deletion of TRPV1 does not completely eliminate these temperature-dependent effects, suggesting involvement of additional thermosensitive ion channels. The warm-sensitive, calcium-permeable, ion channel TRPV3 is commonly expressed with TRPV1; however, the extent to which TRPV3 is found in vagal afferent neurons is unknown. Here, we begin to characterize the genetic and functional expression of TRPV3 in vagal afferent neurons using molecular biology (RT-PCR and RT-quantitative PCR) in whole nodose and isolated neurons and fluorescent calcium imaging on primary cultures of nodose ganglia neurons. We confirmed low-level TRPV3 expression in vagal afferent neurons and observed direct activation with putative TRPV3 agonists eugenol, ethyl vanillin (EVA), and farnesyl pyrophosphate (FPP). Agonist activation stimulated neurons also containing TRPV1 and was blocked by ruthenium red. FPP sensitivity overlapped with EVA and eugenol but represented the smallest percentage of vagal afferent neurons, and it was the only agonist that did not stimulate neurons from TRPV3−/−1 mice, suggesting FPP has the highest selectivity. Further, FPP was predictive of enhanced responses to capsaicin, EVA, and eugenol in rats. From our results, we conclude TRPV3 is expressed in a discrete subpopulation of vagal afferent neurons and may contribute to vagal afferent signaling either directly or in combination with TRPV1.

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