Abdominal vagal afferent pathways and their distributions of intraganglionic laminar endings in the rat duodenum

2012 ◽  
Vol 520 (5) ◽  
pp. 1098-1113 ◽  
Author(s):  
Feng-Bin Wang ◽  
Yao Kuang Young ◽  
Chih-Kuan Kao
Keyword(s):  
Afferent Pathways ◽  
Intraganglionic Laminar Endings ◽  
Rat Duodenum ◽  
Vagal Afferent

Duodenal acid-induced gastric relaxation is mediated by multiple pathways

1999 ◽  
Vol 276 (6) ◽  
pp. G1501-G1506 ◽  
Author(s):  
Yuan-Xu Lu ◽  
Chung Owyang
Keyword(s):  
Gastric Motility ◽  
No Reduction ◽  
Direct Action ◽  
Intragastric Pressure ◽  
Afferent Pathways ◽  
Serotonin Antagonist ◽  
Intraduodenal Infusion ◽  
Rate Dependent ◽  
Vagal Afferent

In this study, we used an in vivo anesthetized rat model to investigate the mechanisms responsible for duodenal acid-induced inhibition of gastric motility. Intraduodenal infusion of HCl produced a rate-dependent decrease in intragastric pressure. Infusion of HCl at 2 ml/h produced a physiological plasma secretin level and elicited a decrease in intragastric pressure of 3.0 ± 0.2 cmH20. Infusion of rabbit secretin antiserum reduced the acid-induced inhibition of gastric motility by 85 ± 5%, suggesting mediation mainly by endogenous secretin. Administration of the cholecystokinin (CCK)-A antagonist MK-329 caused only a modest 10 ± 3% reduction in gastric relaxation, whereas the serotonin antagonist ICS-205930 had no effect. In contrast, immunoneutralization with the secretin antibody caused only a 15% reduction in the relaxation evoked by a higher rate of HCl infusion (3 ml/h), whereas MK-329 and ICS-205930 caused a 20 ± 4% reduction and no reduction, respectively. Bilateral truncal vagotomy or perivagal application of capsaicin completely abolished gastric relaxation in response to low rates (1–2 ml/h) of 0.1 N HCl infusion but only partially affected gastric relaxation in response to a higher infusion rate (3 ml/h). These observations indicate that multiple pathways mediate the duodenal acid-induced inhibition of gastric motility. At low rates of HCl infusion, gastric relaxation is mediated primarily by endogenous secretin, which acts through vagal afferent pathways. At higher rates of HCl infusion, gastric relaxation is mediated by endogenous secretin, CCK, and possibly by the direct action of HCl on vagal afferent pathways or yet unidentified neuropathways.

GABAB receptors on vagal afferent pathways: peripheral and central inhibition

2001 ◽  
Vol 280 (4) ◽  
pp. G658-G668 ◽  
Author(s):  
Elita R. Partosoedarso ◽  
Richard L. Young ◽  
L. Ashley Blackshaw
Keyword(s):  
Brain Stem ◽  
Gabab Receptors ◽  
Vagal Afferents ◽  
Gastric Distension ◽  
Neuronal Responses ◽  
Afferent Pathways ◽  
Central Inhibition ◽  
Vagal Afferent ◽  
Vagal Efferents ◽  
Cgp 35348

To investigate GABAB receptors along vagal afferent pathways, we recorded from vagal afferents, medullary neurons, and vagal efferents in ferrets. Baclofen (7–14 μmol/kg iv) reduced gastric tension receptor and nucleus tractus solitarii neuronal responses to gastric distension but not gastroduodenal mucosal receptor responses to cholecystokinin (CCK). GABAB antagonists CGP-35348 or CGP-62349 reversed effects of baclofen. Vagal efferents showed excitatory and inhibitory responses to distension and CCK. Baclofen (3 nmol icv or 7–14 μmol/kg iv) reduced both distension response types but reduced only inhibitory responses to CCK. CGP-35348 (100 nmol icv or 100 μmol/kg iv) reversed baclofen's effect on distension responses, but inhibitory responses to CCK remained attenuated. They were, however, reversed by CGP-62349 (0.4 nmol icv). In conclusion, GABAB receptors inhibit mechanosensitivity, not chemosensitivity, of vagal afferents peripherally. Mechanosensory input to brain stem neurons is also reduced centrally by GABAB receptors, but excitatory chemosensory input is unaffected. Inhibitory mechano- and chemosensory inputs to brain stem neurons (via inhibitory interneurons) are both reduced, but the pathway taken by chemosensory input involves GABAB receptors that are insensitive to CGP-35348.

Learned flavor preferences induced by intragastric administration of rewarding nutrients: role of capsaicin-sensitive vagal afferent fibers

2007 ◽  
Vol 293 (2) ◽  
pp. R635-R641 ◽  
Author(s):  
Maria A. Zafra ◽  
Filomena Molina ◽  
Amadeo Puerto
Keyword(s):  
Physiological Saline ◽  
Tween 80 ◽  
Daily Basis ◽  
Preference Learning ◽  
Intragastric Administration ◽  
Flavor Preference ◽  
Afferent Pathways ◽  
Afferent Fibers ◽  
Vagal Afferent

Learned flavor preferences can be established after intragastric nutrient administration by two different behavioral procedures, concurrent and sequential. In a concurrent procedure, two flavored stimuli are offered separately but at the same time on a daily basis: one stimulus is paired with the simultaneous intragastric administration of partially digested food and the other with physiological saline. In sequential learning, the two stimuli are presented during alternate sessions. Neural mechanisms underlying these learning modalities have yet to be fully elucidated. The aim of this study was to examine the role of vagal afferent fibers in the visceral processing of rewarding nutrients during concurrent ( experiment 1) and sequential ( experiment 2) flavor preference learning in Wistar rats. For this purpose, capsaicin, a neurotoxin that destroys slightly myelinated or unmyelinated sensory axons, was applied to the subdiaphragmatic region of the esophagus to selectively damage most of the vagal afferent pathways that originate in the gastrointestinal system. Results showed that capsaicin [1 mg of capsaicin dissolved in 1 ml of vehicle (10% Tween 80 in oil)] blocked acquisition of concurrent but not sequential flavor preference learning. These results are interpreted in terms of a dual neurobiological system involved in processing the rewarding effects of intragastrically administered nutrients. The vagus nerve, specifically capsaicin-sensitive vagal afferent fibers, would only be essential in concurrent flavor preference learning, which requires rapid processing of visceral information.

scholarly journals Satiety induced by bile acids is mediated via vagal afferent pathways

JCI Insight ◽  
2020 ◽  
Vol 5 (14) ◽  
Author(s):  
Xiaoyin Wu ◽  
Ji-Yao Li ◽  
Allen Lee ◽  
Yuan-Xu Lu ◽  
Shi-Yi Zhou ◽  
...  
Keyword(s):  
Bile Acids ◽  
Afferent Pathways ◽  
Vagal Afferent

Pancreatic secretion stimulated by CCK is not mediated by capsaicin-sensitive vagal afferent pathway in awake rats

1996 ◽  
Vol 270 (5) ◽  
pp. G881-G886 ◽  
Author(s):  
D. Guan ◽  
W. T. Phillips ◽  
G. M. Green
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Pancreatic Secretion ◽  
Fluid Secretion ◽  
Afferent Pathway ◽  
Afferent Pathways ◽  
Intraduodenal Infusion ◽  
Anesthetized Rats ◽  
Vagal Afferent ◽  
Awake Rats

A capsaicin-sensitive vagal afferent pathway was reported to mediate the effect of endogenous cholecystokinin (CCK) on pancreatic secretion in anesthetized rats. Because neural blockade affects pancreatic secretion much less in awake than in anesthetized rats, the effect of capsaicin ablation of vagal afferent pathways on pancreatic secretion stimulated by endogenous CCK was examined in awake rats. During surgery, abdominal vagal trunks were exposed, and 0.1 ml of capsaicin (10 mg/ml) was applied to the vagal trunks. Ablation of the vagal afferent pathway was assessed by the ability of intraperitoneal cholecystokinin octapeptide (CCK-8) to suppress food intake and inhibit gastric emptying. Endogenous CCK release was stimulated by diversion of bile pancreatic juice from the intestine and by intraduodenal infusion of casein. Pancreatic protein and fluid secretion were significantly increased by both treatments, and the responses were unaffected by capsaicin. Intraperitoneal CCK-8 markedly inhibited food intake and gastric emptying, and both effects were significantly attenuated in capsaicin-treated rats, indicating that capsaicin treatment successfully ablated vagal afferent fibers. It is concluded that CCK-stimulated pancreatic secretion in rats is not mediated by a vagal afferent pathway.

Reflex control of abdominal muscles during positive-pressure breathing

1964 ◽  
Vol 19 (2) ◽  
pp. 224-232 ◽  
Author(s):  
Beverly Bishop
Keyword(s):  
Abdominal Muscle ◽  
Spinal Reflexes ◽  
The Other ◽  
Positive Pressure ◽  
Abdominal Muscles ◽  
Afferent Pathways ◽  
Muscle Response ◽  
Thoracic Spinal ◽  
Vagal Afferent ◽  
Continuous Positive Pressure

Continuous positive-pressure breathing initiates expiratory activity in the abdominal muscle and inhibits the diaphragm in anesthetized cats. This investigation defines neural mechanisms involved in this abdominal muscle response (AMR) to positive-pressure breathing. The AMR is not a segmental reflex since it is abolished by thoracic spinal transection. Bilateral rhizotomy (T8-L3) also eliminates AMR, but laparotomy and abdominal evisceration do not, suggesting that some neural inflow other than from abdominal muscle or viscera is necessary but insufficient for maintaining AMR. Abdominal vagotomy failed to interrupt AMR which was abolished by bilateral cervical vagotomy, indicating that the necessary receptors lie in the thorax. Compression or local anesthesia of the cervical vagi provided the experimental means for abolishing either the inhibition of the diaphragm or the AMR without necessarily interrupting the other. That one response may persist in the absence of the other indicates that vagal afferent pathways subserving AMR are distinct from those mediating diaphragm inhibition. Hence the active expiration of pressure breathing is not a simple corollary of the Hering-Breuer inflation reflex but is a separate reflex served by its own vagal pathway. abdominal muscle response; vagus control of active expiration; abdominal muscle motoneuron pool; vagal afferent pathway in pressure-breathing reflex; thoracic receptors; diaphragm response to pressure breathing; diaphragm; inspiration; expiratory reflexes; inspiratory reflexes; respiratory reflexes; segmental reflexes; spinal reflexes Submitted on February 21, 1963

scholarly journals Ghrelin, Des-Acyl Ghrelin, and Obestatin: Regulatory Roles on the Gastrointestinal Motility

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Mineko Fujimiya ◽  
Akihiro Asakawa ◽  
Koji Ataka ◽  
Chih-Yen Chen ◽  
Ikuo Kato ◽  
...  
Keyword(s):  
Gastrointestinal Motility ◽  
Inhibitory Effects ◽  
Conscious Rat ◽  
Afferent Pathways ◽  
Fed State ◽  
Fasted State ◽  
Vagal Afferent ◽  
Acyl Ghrelin ◽  
The Brain

Ghrelin, des-acyl ghrelin, and obestatin are derived from a common prohormone, preproghrelin by posttranslational processing, originating from endocrine cells in the stomach. To examine the regulatory roles of these peptides, we applied the manometric measurement of gastrointestinal motility in freely moving conscious rat or mouse model. Ghrelin exerts stimulatory effects on the motility of antrum and duodenum in both fed and fasted state of animals. Des-acyl ghrelin exerts inhibitory effects on the motility of antrum but not on the motility of duodenum in the fasted state of animals. Obestatin exerts inhibitory effects on the motility of antrum and duodenum in the fed state but not in the fasted state of animals. NPY Y2 and Y4 receptors in the brain may mediate the action of ghrelin, CRF type 2 receptor in the brain may mediate the action of des-acyl ghrelin, whereas CRF type 1 and type 2 receptors in the brain may mediate the action of obestatin. Vagal afferent pathways might be involved in the action of ghrelin, but not involved in the action of des-acyl ghrelin, whereas vagal afferent pathways might be partially involved in the action of obestatin.

scholarly journals Gastric relaxation induced by hyperglycemia is mediated by vagal afferent pathways in the rat

2008 ◽  
Vol 294 (5) ◽  
pp. G1158-G1164 ◽  
Author(s):  
Shi-Yi Zhou ◽  
Yuan-Xu Lu ◽  
Chung Owyang
Keyword(s):  
Gastric Motility ◽  
Electrical Field Stimulation ◽  
Glucose Sensing ◽  
Vagal Afferents ◽  
Dependent Manner ◽  
Intragastric Pressure ◽  
Synthesis Inhibitor ◽  
Afferent Pathways ◽  
Nodose Ganglia ◽  
Vagal Afferent

Hyperglycemia has a profound effect on gastric motility. However, little is known about the site and mechanism that sense alteration in blood glucose level. The identification of glucose-sensing neurons in the nodose ganglia led us to hypothesize that hyperglycemia acts through vagal afferent pathways to inhibit gastric motility. With the use of a glucose-clamp rat model, we showed that glucose decreased intragastric pressure in a dose-dependent manner. In contrast to intravenous infusion of glucose, intracisternal injection of glucose at 250 and 500 mg/dl had little effect on intragastric pressure. Pretreatment with hexamethonium, as well as truncal vagotomy, abolished the gastric motor responses to hyperglycemia (250 mg/dl), and perivagal and gastroduodenal applications of capsaicin significantly reduced the gastric responses to hyperglycemia. In contrast, hyperglycemia had no effect on the gastric contraction induced by electrical field stimulation or carbachol (10−5 M). To rule out involvement of serotonergic pathways, we showed that neither granisetron (5-HT3 antagonist, 0.5 g/kg) nor pharmacological depletion of 5-HT using p-chlorophenylalanine (5-HT synthesis inhibitor) affected gastric relaxation induced by hyperglycemia. Lastly, NG-nitro-l-arginine methyl ester (l-NAME) and a VIP antagonist each partially reduced gastric relaxation induced by hyperglycemia and, in combination, completely abolished gastric responses. In conclusion, hyperglycemia inhibits gastric motility through a capsaicin-sensitive vagal afferent pathway originating from the gastroduodenal mucosa. Hyperglycemia stimulates vagal afferents, which, in turn, activate vagal efferent cholinergic pathways synapsing with intragastric nitric oxide- and VIP-containing neurons to mediate gastric relaxation.

Distribution and structure of vagal afferent intraganglionic laminar endings (IGLEs) in the rat gastrointestinal tract

1997 ◽  
Vol 195 (2) ◽  
pp. 183-191 ◽  
Author(s):  
H.-R. Berthoud ◽  
Laurel M. Patterson ◽  
Friederike Neumann ◽  
Winfried L. Neuhuber
Keyword(s):  
Gastrointestinal Tract ◽  
Intraganglionic Laminar Endings ◽  
Vagal Afferent
Sign in / Sign up

Export Citation Format

Share Document