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1
Schwartz, G. J., T. H. Moran, W. O. White, and E. E. Ladenheim. "Relationships between gastric motility and gastric vagal afferent responses to CCK and GRP in rats differ." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 6 (June 1, 1997): R1726—R1733. http://dx.doi.org/10.1152/ajpregu.1997.272.6.r1726.
Повний текст джерелаАнотація:
The brain-gut peptides cholecystokinin (CCK) and the mammalian bombesin-like peptide gastrin-releasing peptide (GRP) suppress food intake. Vagotomy blocks CCK- but not bombesin (BN)-induced feeding suppression, demonstrating differential vagal contributions. We examined the relationship between the ability of CCK and the active fragment of GRP, GRP-(18-27), to stimulate gastric vagal afferent activity and their ability to elicit changes in gastric motility. We also examined ligated cervical vagal segments and revealed specific 125I-CCK vagal binding without evidence of radiolabeled BN binding sites. Both close arterial and intraperitoneal CCK and GRP-(18-27) produced dose-dependent increases in activity in gastric vagal mechanoreceptive afferents. CCK dose dependently decreased gastric pressure without altering antral wall tension, whereas GRP-(18-27) dose dependently increased both gastric pressure and peak antral wall muscle tension. These results suggest that GRP-(18-27) activates gastric vagal afferents secondary to its stimulation of gastric motor effects. CCK activates this same population of vagal afferents independent of changes in gastric tension, suggesting a direct action of CCK at functional vagal CCK receptors.
2
van de Wall, E. H. E. M., P. Duffy, and R. C. Ritter. "CCK enhances response to gastric distension by acting on capsaicin-insensitive vagal afferents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 3 (September 2005): R695—R703. http://dx.doi.org/10.1152/ajpregu.00809.2004.
Повний текст джерелаАнотація:
Capsaicin treatment destroys vagal afferent C fibers and markedly attenuates reduction of food intake and induction of hindbrain Fos expression by CCK. However, both anatomical and electrophysiological data indicate that some gastric vagal afferents are not destroyed by capsaicin. Because CCK enhances behavioral and electrophysiological responses to gastric distension in rats and people, we hypothesized that CCK might enhance the vagal afferent response to gastric distension via an action on capsaicin-insensitive vagal afferents. To test this hypothesis, we quantified expression of Fos-like immunoreactivity (Fos) in the dorsal vagal complex (DVC) of capsaicin-treated (Cap) and control rats (Veh), following gastric balloon distension alone and in combination with CCK injection. In Veh rats, intraperitoneal CCK significantly increased DVC Fos, especially in nucleus of the solitary tract (NTS), whereas in Cap rats, CCK did not significantly increase DVC Fos. In contrast to CCK, gastric distension did significantly increase Fos expression in the NTS of both Veh and Cap rats, although distension-induced Fos was attenuated in Cap rats. When CCK was administered during gastric distension, it significantly enhanced NTS Fos expression in response to distension in Cap rats. Furthermore, CCK's enhancement of distension-induced Fos in Cap rats was reversed by the selective CCK-A receptor antagonist lorglumide. We conclude that CCK directly activates capsaicin-sensitive C-type vagal afferents. However, in capsaicin-resistant A-type afferents, CCK's principal action may be facilitation of responses to gastric distension.
3
Raybould, Helen E., Jorg Glatzle, Carla Robin, James H. Meyer, Thomas Phan, Helen Wong, and Catia Sternini. "Expression of 5-HT3 receptors by extrinsic duodenal afferents contribute to intestinal inhibition of gastric emptying." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 3 (March 1, 2003): G367—G372. http://dx.doi.org/10.1152/ajpgi.00292.2001.
Повний текст джерелаАнотація:
Intestinal perfusion with carbohydrates inhibits gastric emptying via vagal and spinal capsaicin-sensitive afferent pathways. The aim of the present study was to determine the role of 1) 5-hydroxytryptamine (5-HT)3receptors (5-HT3R) in mediating glucose-induced inhibition of gastric emptying and 2) 5-HT3R expression in vagal and spinal afferents in innervating the duodenum. In awake rats fitted with gastric and duodenal cannulas, perfusion of the duodenum with glucose (50 and 100 mg) inhibited gastric emptying. Intestinal perfusion of mannitol inhibited gastric emptying only at the highest concentration (990 mosm/kgH2O). Pretreatment with the 5-HT3R antagonist tropisetron abolished both glucose- and mannitol-induced inhibition of gastric emptying. Retrograde labeling of visceral afferents by injection of dextran-conjugated Texas Red into the duodenal wall was used to identify extrinsic primary afferents. Immunoreactivity for 5-HT3R, visualized with an antibody directed to the COOH terminus of the rat 5-HT3R, was found in >80% of duodenal vagal and spinal afferents. These results show that duodenal extrinsic afferents express 5-HT3R and that the receptor mediates specific glucose-induced inhibition of gastric emptying. These findings support the hypothesis that enterochromaffin cells in the intestinal mucosa release 5-HT in response to glucose, which activates 5-HT3R on afferent nerve terminals to evoke reflex changes in gastric motility. The primary glucose sensors of the intestine may be mucosal enterochromaffin cells.
4
Smid, Scott D., Richard L. Young, Nicole J. Cooper, and L. Ashley Blackshaw. "GABABR expressed on vagal afferent neurones inhibit gastric mechanosensitivity in ferret proximal stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 6 (December 1, 2001): G1494—G1501. http://dx.doi.org/10.1152/ajpgi.2001.281.6.g1494.
Повний текст джерелаАнотація:
GABAB-receptor (GABABR) agonists reduce transient lower esophageal sphincter relaxation (TLESR) and reflux episodes through an action on vagal pathways. In this study, we determined whether GABABR are expressed on vagal afferent neurones and whether they modulate distension-evoked discharge of vagal afferents in the isolated stomach. Vagal mehanoreceptor activity was recorded following distensions of the isolated ferret proximal stomach before and after perfusion with the GABABR-selective agonists baclofen and 3-aminopropylphosphinic acid (3-APPiA). Retrograde labeling and immunohistochemistry were used to identify GABABR located on vagal afferent neurones in the nodose ganglia. Vagal afferent fibers responded to isovolumetric gastric distension with an increase in discharge. The GABAB-receptor agonists baclofen (5 × 10−5 M) and 3-APPiA (10−6 to 10−5 M) but not muscimol (GABAA-selective agonist: 1.3 × 10−5 M) significantly decreased afferent distension-response curves. The effect of baclofen (5 × 10−5 M) was reversed by the GABAB-receptor antagonist CGP 62349 (10−5 M). Over 93% of retrogradely labeled gastric vagal afferents in the nodose ganglia expressed immunoreactivity for the GABABR. GABABR expressed on vagal afferent fibers directly inhibit gastric mechanosensory activity. This is likely a contributing mechanism to the efficacy of GABAB-receptor agonists in reducing TLESR and reflux episodes in vivo.
5
Mathis, Carole, Timothy H. Moran, and Gary J. Schwartz. "Load-sensitive rat gastric vagal afferents encode volume but not gastric nutrients." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 2 (February 1, 1998): R280—R286. http://dx.doi.org/10.1152/ajpregu.1998.274.2.r280.
Повний текст джерелаАнотація:
To assess nutrient sensitivity in a population of gastric load-sensitive vagal afferents, their neurophysiological activity was examined in anesthetized rats with inflated pyloric cuffs after gastric infusion of a range of volumes of nutrient and equiosmotic saline solutions. Responses to physiological saline loads (1, 2, 4, and 8 ml) were compared with responses elicited by the same volume range of carbohydrate (12.5% glucose), protein (12.5% peptone), and equiosmotic hypertonic (750 mosM) saline. The threshold load volume of physiological saline required to increase gastric vagal afferent activity was 1 ml. Thereafter, there was a dose-dependent relationship between increasing gastric volume and firing rate and between gastric volume and pressure. The dose-response relationships elicited by glucose, peptone, and equiosmotic hypertonic saline loads did not differ from those elicited by physiological saline loads. These data identify a population of gastric load-sensitive vagal afferents unresponsive to the chemical composition of gastric contents and are consistent with a role for vagal gastric volume signals but not gastric nutrient content in the negative feedback control of ingestion.
6
Kang, Yu-Ming, Klaus Bielefeldt, and G. F. Gebhart. "Sensitization of Mechanosensitive Gastric Vagal Afferent Fibers in the Rat by Thermal and Chemical Stimuli and Gastric Ulcers." Journal of Neurophysiology 91, no. 5 (May 2004): 1981–89. http://dx.doi.org/10.1152/jn.01097.2003.
Повний текст джерелаАнотація:
In the present study we examined the effects of acute thermal and chemical stimuli and gastric ulceration on mechanosensitive gastric vagal afferent fibers. Single-fiber recordings were made from the cervical vagus nerve. Mechanosensitive afferent fibers were identified by response to gastric distension (GD). Intragastric pressure was maintained below 3 mmHg during intragastric instillation of saline, heated saline, HCl, or glycocholic acid. Responses to graded GD (5–60 mmHg, 20 s, 4-min interval) were determined before and after 30-min exposure to thermal or chemical stimuli. All mechanosensitive fibers studied were C-fibers (mean CV: 1.07 ± 0.07 m/s). Saline (37°C) did not affect resting activity or alter responses to GD, but exposure to heated saline (46°C) significantly increased resting activity and sensitized responses to GD. The decrease in resting activity was hydrochloric acid concentration dependent (0.025–0.2 N), but responses to GD were sensitized after 30-min exposure to 0.1 N HCl ( n = 7). The bile acid glycocholic acid significantly increased resting activity and desensitized responses to GD at an intragastric pH of 7, and similarly increased resting activity but sensitized responses to GD ( n = 6) at an intragastric pH of 1.2. Vagal afferents recorded in rats with gastric ulcers had significantly greater resting activity and responses to GD than sham ulcer rats; intragastric instillation of glycocholic acid (pH 1.2) further increased afferent fiber excitability. These findings indicate that acute gastric thermal and chemical stimuli alter the response characteristics of mechanosensitive vagal afferents in the absence of inflammation or structural damage. Accordingly, acute sensitization of gastric afferents through different stimulus modalities may contribute to the development of dyspeptic symptoms. In the presence of gastric inflammation, mechanosensitive vagal afferents exhibit a further increase in excitability.
7
Young, Richard L., Amanda J. Page, Tracey A. O'Donnell, Nicole J. Cooper, and L. Ashley Blackshaw. "Peripheral versus central modulation of gastric vagal pathways by metabotropic glutamate receptor 5." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 2 (February 2007): G501—G511. http://dx.doi.org/10.1152/ajpgi.00353.2006.
Повний текст джерелаАнотація:
Metabotropic glutamate receptors (mGluR) are classified into group I, II, and III mGluR. Group I (mGluR1, mGluR5) are excitatory, whereas group II and III are inhibitory. mGluR5 antagonism potently reduces triggering of transient lower esophageal sphincter relaxations and gastroesophageal reflux. Transient lower esophageal sphincter relaxations are mediated via a vagal pathway and initiated by distension of the proximal stomach. Here, we determined the site of action of mGluR5 in gastric vagal pathways by investigating peripheral responses of ferret gastroesophageal vagal afferents to graded mechanical stimuli in vitro and central responses of nucleus tractus solitarius (NTS) neurons with gastric input in vivo in the presence or absence of the mGluR5 antagonist 2-methyl-6-(phenylethynyl)pyridine (MPEP). mGluR5 were also identified immunohistochemically in the nodose ganglia and NTS after extrinsic vagal inputs had been traced from the proximal stomach. Gastroesophageal vagal afferents were classified as mucosal, tension, or tension-mucosal (TM) receptors. MPEP (1–10 μM) inhibited responses to circumferential tension of tension and TM receptors. Responses to mucosal stroking of mucosal and TM receptors were unaffected. MPEP (0.001–10 nmol icv) had no major effect on the majority of NTS neurons excited by gastric distension or on NTS neurons inhibited by distension. mGluR5 labeling was abundant in gastric vagal afferent neurons and sparse in fibers within NTS vagal subnuclei. We conclude that mGluR5 play a prominent role at gastroesophageal vagal afferent endings but a minor role in central gastric vagal pathways. Peripheral mGluR5 may prove a suitable target for reducing mechanosensory input from the periphery, for therapeutic benefit.
8
Schwartz, Gary J., and Timothy H. Moran. "Duodenal nutrient exposure elicits nutrient-specific gut motility and vagal afferent signals in rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 5 (May 1, 1998): R1236—R1242. http://dx.doi.org/10.1152/ajpregu.1998.274.5.r1236.
Повний текст джерелаАнотація:
Volume and chemical characteristics of meals in the gut have been proposed to generate vagal afferent signals that mediate the negative feedback control of ingestion and gastric emptying. Furthermore, duodenal nutrients elicit changes in gastrointestinal motility that may stimulate mechanosensitive vagal afferents. The degree to which the activity of an individual vagal afferent fiber can be modified by both mechanical and nutrient properties in the gut remains unclear. The present studies evaluated the relationships between distal antral and proximal duodenal load-sensitive vagal afferent activity and gastroduodenal motility in response to duodenal nutrient exposure in ketamine-xylazine-anesthetized rats. Duodenal carbohydrate (glucose) and amino acid (peptone) infusions (0.2 ml/min, 0.2–0.5 kcal/ml) stimulated concentration-dependent increases in 1) antroduodenal contractions and 2) antral and duodenal vagal afferent activity beyond those attributable to osmolarity alone. In addition, duodenal peptone was more effective than equicaloric glucose in eliciting this vagal activity. These data demonstrate that the proximal duodenum can discriminate its nutrient chemical contents and that gastroduodenal load-sensitive vagal afferents indirectly transduce nutrient chemical information.
9
Schwartz, G. J., P. R. McHugh, and T. H. Moran. "Pharmacological dissociation of responses to CCK and gastric loads in rat mechanosensitive vagal afferents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (July 1, 1994): R303—R308. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r303.
Повний текст джерелаАнотація:
To identify the transduction mechanisms underlying gastric vagal afferent responses to gastric loads and cholecystokinin (CCK), we investigated the ability of specific CCK antagonists, acute pylorectomy, and cholinergic blockade to effect these vagal afferent responses. The CCK-B antagonist L-365,260 (10 pmol-1 nmol) failed to block the gastric vagal afferent response to gastric loads or 100 pmol CCK, while the CCK-A antagonist devazepide (100 pmol-100 nmol) competitively and dose dependently attenuated the response to CCK but not to gastric loads. Application of 100 nmol of the low-affinity CCK receptor antagonist CCK-JMV-180 also completely blocked the gastric vagal afferent response to 100 pmol CCK. Acute pylorectomy failed to block the gastric vagal afferent response to 100 pmol CCK or 2-ml gastric loads. Atropine sulfate administration (15 mg/rat) failed to block the gastric vagal afferent response to 100 pmol CCK or 2-ml gastric loads. These data suggest that 1) the vagal afferent response to CCK is mediated through CCK's interactions with vagal, rather than pyloric, CCK-A receptors, and 2) the vagal afferent responses to CCK and to gastric loads are mediated by dissociable, possibly independent, transduction mechanisms.
10
Danzer, Marion, Milana Jocic, Claudia Samberger, Evelin Painsipp, Elisabeth Bock, Maria-Anna Pabst, Karl Crailsheim, Rudolf Schicho, Irmgard T. Lippe, and Peter Holzer. "Stomach-brain communication by vagal afferents in response to luminal acid backdiffusion, gastrin, and gastric acid secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 3 (March 2004): G403—G411. http://dx.doi.org/10.1152/ajpgi.00308.2003.
Повний текст джерелаАнотація:
Vagal afferents play a role in gut-brain signaling of physiological and pathological stimuli. Here, we investigated how backdiffusion of luminal HCl or NH4OH and pentagastrin-stimulated acid secretion interact in the communication between rat stomach and brain stem. Rats were pretreated intraperitoneally with vehicle or appropriate doses of cimetidine, omeprazole, pentagastrin, dexloxiglumide (CCK1 receptor antagonist), and itriglumide (CCK2 receptor antagonist) before intragastric administration of saline or backdiffusing concentrations of HCl or NH4OH. Two hours later, neuronal activation in the nucleus of the solitary tract (NTS) and area postrema was visualized by c-Fos immunohistochemistry. Exposure of the rat gastric mucosa to HCl (0.15-0.5 M) or NH4OH (0.1-0.3 M) led to a concentration-dependent expression of c-Fos in the NTS, which was not related to gender, gastric mucosal injury, or gastropyloric motor alterations. The c-Fos response to HCl was diminished by cimetidine and omeprazole, enhanced by pentagastrin, and left unchanged by dexloxiglumide and itriglumide. Pentagastrin alone caused an omeprazole-resistant expression of c-fos, which in the NTS was attenuated by itriglumide and prevented by dexloxiglumide but in the area postrema was reduced by dexloxiglumide and abolished by itriglumide. We conclude that vagal afferents transmit physiological stimuli (gastrin) and pathological events (backdiffusion of luminal HCl or NH4OH) from the stomach to the brain stem. These communication modalities interact because, firstly, acid secretion enhances afferent signaling of gastric acid backdiffusion and, secondly, gastrin activates NTS neurons through stimulation of CCK1 receptors on vagal afferents and of CCK2 receptors on area postrema neurons projecting to the NTS.
11
Page, Amanda J., James A. Slattery, Catherine Milte, Rhianna Laker, Tracey O'Donnell, Camilla Dorian, Stuart M. Brierley, and L. Ashley Blackshaw. "Ghrelin selectively reduces mechanosensitivity of upper gastrointestinal vagal afferents." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 5 (May 2007): G1376—G1384. http://dx.doi.org/10.1152/ajpgi.00536.2006.
Повний текст джерелаАнотація:
Ghrelin is a peptide released from gastric endocrine cells that has an orexigenic effect via a vagal pathway. Here we determine the effect of ghrelin on mechanosensitivity of upper-intestinal vagal afferent fibers in ferret and mouse. The responses of gastroesophageal vagal afferents to graded mechanical stimulation were determined in vitro before and during application of ghrelin to their peripheral endings. Three types of vagal afferent were tested: tension receptors responding to circumferential tension, mucosal receptors responding only to mucosal stroking, and tension/mucosal (TM) receptors in ferret esophagus that responded to both stimuli. In the mouse, ghrelin did not significantly affect the response of mucosal receptors to mucosal stroking with calibrated von Frey hairs. However, it significantly reduced responses of tension receptors to circumferential tension ( P < 0.005; two-way ANOVA) by up to 40%. This inhibition was reversed by the ghrelin receptor antagonist [d-Lys-3]-growth hormone-releasing peptide (GHRP)-6. In the ferret, ghrelin significantly reduced the response of mucosal and TM receptors to mucosal stroking with calibrated von Frey hairs. Surprisingly, ghrelin did not significantly alter the response to circumferential tension in either tension or TM receptors. RT-PCR analysis indicated that both ghrelin and its receptor are expressed in vagal afferent cell bodies in mouse nodose ganglia. In conclusion, ghrelin selectively inhibits subpopulations of mechanically sensitive gastroesophageal vagal afferents; there is also potential for ghrelin release from vagal afferents. However, the subpopulation of afferents inhibited differs between species. These data have broad implications for ghrelin's role in food intake regulation and reflex control of gastrointestinal function.
12
Schwartz, G. J., P. R. McHugh, and T. H. Moran. "Gastric loads and cholecystokinin synergistically stimulate rat gastric vagal afferents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 4 (October 1, 1993): R872—R876. http://dx.doi.org/10.1152/ajpregu.1993.265.4.r872.
Повний текст джерелаАнотація:
Both gastric preloads and exogenous cholecystokinin (CCK) administration inhibit food intake, and combinations of preloads and CCK suppress feeding to a greater degree than either stimulus delivered alone. A role for the vagus nerve in mediating CCK's inhibition of food intake has been proposed, and gastric vagal afferent fibers respond to both gastric loads and local CCK infusions. To examine whether combined load and CCK stimuli may synergistically augment gastric neural afferent activity at the level of the peripheral vagus, we have examined the gastric vagal afferent responses (n = 8) to a range of gastric saline loads (1, 2, and 3 ml) and exogenous close celiac arterial CCK (10 and 100 pmol) when administered alone or in combination. Gastric loads ineffective in eliciting a significant increase in vagal afferent activity when administered alone became effective when combined with doses of CCK that were subthreshold for the production of a vagal afferent response. Gastric loads that alone were effective in producing a significant vagal afferent response yielded an even greater response when administered in combination with both subthreshold and suprathreshold doses of CCK. These data demonstrate that, in rats, signals produced by combined gastric load and exogenous CCK administration are integrated peripherally and interact synergistically. These results suggest that signals arising from the vagus may provide sufficient information for the synergistic inhibition of food intake produced by combinations of gastric loads and exogenous CCK.
13
Barber, W. D., and C. S. Yuan. "Brain stem responses to electrical stimulation of ventral vagal gastric fibers." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 1 (July 1, 1989): G24—G29. http://dx.doi.org/10.1152/ajpgi.1989.257.1.g24.
Повний текст джерелаАнотація:
The brain stem neuronal responses to electrical stimulation of gastric branches of the ventral vagal trunk serving the proximal stomach were localized and evaluated in anesthetized cats. The responses were equally distributed bilaterally in the region of nucleus solitarius in the caudal brain stem. The mean latency of the response was 289 +/- 46 (SD) ms, which translated into a conduction velocity of less than 1 m/s based on the distance between the stimulating and recording electrodes. The responses consisted of single and multiple spikes that showed slight variability in the latency, indicating orthodromic activation via a synapse in approximately 98% of the responses recorded. Forty two percent of the units tested showed evidence of convergence of input from vagal afferent fibers in different branches of the ventral vagal trunk that served the proximal stomach. The resultant activity pattern of the unitary response appeared to be the product of 1) the gastric sensory input or modality conveyed by the afferent source and 2) the time of arrival and diversity of modalities served by other gastric afferents impinging on the unit. This provides a mechanism capable of responding on the basis of specific sensory modalities that dynamically reflect ongoing events monitored and conveyed by other gastric afferents in the region.
14
Cao, Jiayue, Xiaokai Wang, Terry L. Powley, and Zhongming Liu. "Gastric neurons in the nucleus tractus solitarius are selective to the orientation of gastric electrical stimulation." Journal of Neural Engineering 18, no. 5 (October 1, 2021): 056066. http://dx.doi.org/10.1088/1741-2552/ac2ec6.
Повний текст джерелаАнотація:
Abstract Objective. Gastric electrical stimulation (GES) is a bioelectric intervention for gastroparesis, obesity, and other functional gastrointestinal disorders. In a potential mechanism of action, GES activates the nerve endings of vagal afferent neurons and induces the vago-vagal reflex through the nucleus tractus solitarius (NTS) in the brainstem. However, it is unclear where and how to stimulate in order to optimize the vagal afferent responses. Approach. To address this question with electrophysiology in rats, we applied mild electrical currents to two serosal targets on the distal forestomach with dense distributions of vagal intramuscular arrays (IMAs) that innervated the circular and longitudinal smooth muscle layers. During stimulation, we recorded single and multi-unit responses from gastric neurons in NTS and evaluated how the recorded responses depended on the stimulus orientation and amplitude. Main results. We found that NTS responses were highly selective to the stimulus orientation for a range of stimulus amplitudes. The strongest responses were observed when the applied current flowed in the same direction as the IMAs in parallel with the underlying smooth muscle fibers. Our results suggest that gastric neurons in NTS may encode the orientation-specific activity of gastric smooth muscles relayed by vagal afferent neurons. Significance. This finding suggests that the orientation of GES is critical to effective engagement of vagal afferents and should be considered in light of the structural phenotypes of vagal terminals in the stomach.
15
Bielefeldt, Klaus, Fang Zhong, H. Richard Koerber, and Brian M. Davis. "Phenotypic characterization of gastric sensory neurons in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 5 (November 2006): G987—G997. http://dx.doi.org/10.1152/ajpgi.00080.2006.
Повний текст джерелаАнотація:
Recent studies suggest that the capsaicin receptor [transient receptor potential vanilloid (TRPV)1] may play a role in visceral mechanosensation. To address the potential role of TRPV1 in vagal sensory neurons, we developed a new in vitro technique allowing us to determine TRPV1 expression directly in physiologically characterized gastric sensory neurons. Stomach, esophagus, and intact vagus nerve up to the central terminations were carefully dissected and placed in a perfusion chamber. Intracellular recordings were made from the soma of nodose neurons during mechanical stimulation of the stomach. Physiologically characterized neurons were labeled iontophoretically with neurobiotin and processed for immunohistochemical experiments. As shown by action potential responses triggered by stimulation of the upper thoracic vagus with a suction electrode, essentially all abdominal vagal afferents in mice conduct in the C-fiber range. Mechanosensitive gastric afferents encode stimulus intensities over a wide range without apparent saturation when punctate stimuli are used. Nine of 37 mechanosensitive vagal afferents expressed TRPV1 immunoreactivity, with 8 of the TRPV1-positive cells responding to stretch. A small number of mechanosensitive gastric vagal afferents express neurofilament heavy chains and did not respond to stretch. By maintaining the structural and functional integrity of vagal afferents up to the nodose ganglion, physiological and immunohistochemical properties of mechanosensory gastric sensory neurons can be studied in vitro. Using this novel technique, we identified TRPV1 immunoreactivity in only one-fourth of gastric mechanosensitive neurons, arguing against a major role of this ion channel in sensation of mechanical stimuli under physiological conditions.
16
Partosoedarso, Elita R., Richard L. Young, and L. Ashley Blackshaw. "GABAB receptors on vagal afferent pathways: peripheral and central inhibition." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 4 (April 1, 2001): G658—G668. http://dx.doi.org/10.1152/ajpgi.2001.280.4.g658.
Повний текст джерелаАнотація:
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.
17
Grabauskas, Gintautas, Shi-Yi Zhou, Yuanxu Lu, Il Song, and Chung Owyang. "Essential Elements for Glucosensing by Gastric Vagal Afferents: Immunocytochemistry and Electrophysiology Studies in the Rat." Endocrinology 154, no. 1 (January 1, 2013): 296–307. http://dx.doi.org/10.1210/en.2012-1382.
Повний текст джерелаАнотація:
Glucosensing nodose ganglia neurons mediate the effects of hyperglycemia on gastrointestinal motility. We hypothesized that the glucose-sensing mechanisms in the nodose ganglia are similar to those of hypothalamic glucose excited neurons, which sense glucose through glycolysis. Glucose metabolism leads to ATP-sensitive potassium channel (KATP) channel closure and membrane depolarization. We identified glucosensing elements in the form of glucose transporters (GLUTs), glucokinase (GK), and KATP channels in rat nodose ganglia and evaluated their physiological significance. In vitro stomach-vagus nerve preparations demonstrated the gastric vagal afferent response to elevated glucose. Western blots and RT-PCR revealed the presence of GLUT1, GLUT3, GLUT4, GK, and Kir6.2 in nodose ganglia neurons and gastric branches of the vagus nerve. Immunocytochemistry confirmed the expression of GLUT3, GK, and Kir6.2 in nodose ganglia neurons (46.3 ± 3%). Patch-clamp studies detected glucose excitation in 30% (25 of 83) of gastric-projecting nodose ganglia neurons, which was abolished by GLUT3 or GK short hairpin RNA transfections. Silencing GLUT1 or GLUT4 in nodose ganglia neurons did not prevent the excitatory response to glucose. Elevated glucose elicited a response from 43% of in vitro nerve preparations. A dose-dependent response was observed, reaching maximum at a glucose level of 250 mg/dl. The gastric vagal afferent responses to glucose were inhibited by diazoxide, a KATP channel opener. In conclusion, a subset of neurons in the nodose ganglia and gastric vagal afferents are glucoresponsive. Glucosensing requires a GLUT, GK, and KATP channels. These elements are transported axonally to the gastric vagal afferents, which can be activated by elevated glucose through modulation of KATP channels.
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Peles, Shachar, Jaime Petersen, Ricardo Aviv, Shai Policker, Ossama Abu-Hatoum, Shlomo A. Ben-Haim, David D. Gutterman, and Jyoti N. Sengupta. "Enhancement of antral contractions and vagal afferent signaling with synchronized electrical stimulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 3 (September 2003): G577—G585. http://dx.doi.org/10.1152/ajpgi.00109.2003.
Повний текст джерелаАнотація:
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.
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Whited, K. L., D. Thao, K. C. Kent Lloyd, A. S. Kopin, and H. E. Raybould. "Targeted disruption of the murine CCK1 receptor gene reduces intestinal lipid-induced feedback inhibition of gastric function." American Journal of Physiology-Gastrointestinal and Liver Physiology 291, no. 1 (July 2006): G156—G162. http://dx.doi.org/10.1152/ajpgi.00569.2005.
Повний текст джерелаАнотація:
Cholecystokinin (CCK), acting at CCK1 receptors (CCK1Rs) on intestinal vagal afferent terminals, has been implicated in the control of gastrointestinal function and food intake. Using CCK1R−/− mice, we tested the hypothesis that lipid-induced activation of the vagal afferent pathway and intestinal feedback of gastric function is CCK1R dependent. In anesthetized CCK1R+/+ (“wild type”) mice, meal-stimulated gastric acid secretion was inhibited by intestinal lipid infusion; this was abolished in CCK1R−/− mice. Gastric emptying of whole egg, measured by nuclear scintigraphy in awake mice, was significantly faster in CCK1R−/− than CCK1R+/+ mice. Gastric emptying of chow was significantly slowed in response to administration of CCK-8 (22 pmol) in CCK1R+/+ but not CCK1R−/− mice. Activation of the vagal afferent pathway was measured by immunohistochemical localization of Fos protein in the nucleus of the solitary tract (NTS; a region where vagal afferents terminate). CCK-8 (22 pmol ip) increased neuronal Fos expression in the NTS of fasted CCK1R+/+ mice; CCK-induced Fos expression was reduced by 97% in CCK1R−/− compared with CCK1R+/+ mice. Intralipid (0.2 ml of 20% Intralipid and 0.04 g lipid), but not saline, gavage increased Fos expression in the NTS of fasted CCK1R+/+ mice; lipid-induced Fos expression was decreased by 47% in CCK1R−/− compared with CCK1R+/+mice. We conclude that intestinal lipid activates the vagal afferent pathway, decreases gastric acid secretion, and delays gastric emptying via a CCK1R-dependent mechanism. Thus, despite a relatively normal phenotype, intestinal feedback in response to lipid is severely impaired in these mice.
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Holzer, H. H., and H. E. Raybould. "Vagal and splanchnic sensory pathways mediate inhibition of gastric motility induced by duodenal distension." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 4 (April 1, 1992): G603—G608. http://dx.doi.org/10.1152/ajpgi.1992.262.4.g603.
Повний текст джерелаАнотація:
Afferent pathways mediating gastric corpus relaxation after duodenal distension were studied in urethan-anesthetized rats in which the sensory neurotoxin capsaicin (1%) or its vehicle was applied directly to the cervical vagus nerve trunks or the celiac-superior mesenteric ganglia 10-20 days before experiments. Distension (0.05-0.5 ml) of a closed loop of proximal duodenum decreased gastric intraluminal pressure. Perineural capsaicin treatment to the vagus nerves decreased by 73 and 80% the response to low volumes of distension (0.05 and 0.1 ml). Perineural capsaicin treatment of the celiac-superior mesenteric ganglia significantly attenuated by 46-88% the response to all volumes of distension. Bilateral cervical vagotomy or ganglionectomy reduced the response to all volumes of duodenal distension and, in combination, abolished the response. It is concluded that the decrease in gastric corpus motility after duodenal distension is dependent on the extrinsic innervation to the upper gastrointestinal tract and is mediated by both vagal and spinal capsaicin-sensitive afferents. Capsaicin-sensitive vagal afferents mediate responses to low volumes of distension that may be physiological. Capsaicin-sensitive spinal afferents mediate the gastric response to higher volumes of distension and may be involved in mediating visceral and somatic responses to pathophysiological intestinal obstruction.
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Yuan, C. S., and W. D. Barber. "Hypothalamic unitary responses to gastric vagal input from the proximal stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 1 (January 1, 1992): G74—G80. http://dx.doi.org/10.1152/ajpgi.1992.262.1.g74.
Повний текст джерелаАнотація:
Gastric vagally evoked extracellular unitary responses were recorded in the hypothalamus of anesthetized cats. The evoked unitary responses were localized in the paraventricular dorsomedial region, ventromedial nucleus, and lateral hypothalamus. The mean latency of the gastric vagally evoked hypothalamic neuronal responses in these three areas ranged from 368 +/- 39.8 to 371 +/- 45.2 (SD) ms. The majority (82%) of the gastric vagally evoked hypothalamic responses consisted of one to five spikes, while the remaining 18% were tonically active units. The vagal effect was inhibitory in 78% of the tonically active hypothalamic units responding to gastric vagal input. Convergence of gastric vagal input on single hypothalamic units from afferents in the dorsal and ventral vagal trunks was observed. Units were identified in the hypothalamus that responded to activation of mechanoreceptors in the proximal stomach by an intragastric balloon. This study provided new direct evidence of the density, localization, and characteristics of neuronal processing of gastric vagal input from the proximal stomach in the hypothalamus. The reciprocal connections between these areas of the hypothalamus and nucleus tractus solitarius in the caudal brain stem suggest that the hypothalamus may serve an important role in modulating the input of primary vagal afferent input from the proximal stomach.
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Zhou, Shi-Yi, Yuan-Xu Lu, and Chung Owyang. "Gastric relaxation induced by hyperglycemia is mediated by vagal afferent pathways in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 5 (May 2008): G1158—G1164. http://dx.doi.org/10.1152/ajpgi.00067.2008.
Повний текст джерелаАнотація:
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.
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Kobashi, Motoi, Tomoshige Koga, Masatoshi Mizutani, and Ryuji Matsuo. "Suppression of vagal motor activities evokes laryngeal afferent-mediated inhibition of gastric motility." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 3 (March 1, 2002): R818—R827. http://dx.doi.org/10.1152/ajpregu.00180.2001.
Повний текст джерелаАнотація:
We previously reported that the activation of water-responsive afferents in the superior laryngeal nerve was responsible for the inhibition of gastric motility. The present study was undertaken to clarify the roles of the vagal preganglionic neurons responsible for laryngeal afferent-mediated inhibition of gastric motility. Intravenous injection of atropine abolished the inhibition of motility in both the distal and the proximal stomach induced by water administration into the larynx. The neurons in the dorsal motor nucleus of the vagus (DMV), which project to the abdominal viscera, were exclusively inhibited by water administration. Taken together, inhibition of neurons in the DMV induces inhibition of gastric motility evoked by laryngeal water-responsive afferents via a cholinergic pathway. Because chemical lesions of the intermediate DMV, but not the caudal DMV, abolished the inhibition of the distal stomach motility induced by water administration, the intermediate DMV is responsible for the inhibition shown in the distal stomach.
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Hierlihy, L. E., J. L. Wallace, and A. V. Ferguson. "Vagal stimulation-induced gastric damage in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 261, no. 1 (July 1, 1991): G104—G110. http://dx.doi.org/10.1152/ajpgi.1991.261.1.g104.
Повний текст джерелаАнотація:
The role of the vagus nerve in the development of gastric mucosal damage was examined in urethan-anesthetized male Sprague-Dawley rats. Electrical stimulation was applied to the vagus nerves for a period of 60 min, after which macroscopic gastric damage was scored and samples of the stomach were fixed for later histological assessment. Damage scores were assigned blindly based on a 0 (normal) to 3 (severe) scale. Stimulation of vagal afferents or efferents in isolation did not result in significant damage to the gastric mucosa (P greater than 0.1). In contrast, stimulation of both intact vagus nerves resulted in significant gastric mucosal damage (mean damage score, 2.0 +/- 0.33, P less than 0.01). A second series of experiments demonstrated this gastric damage to be induced within 30-60 min; extending the stimulation period to 120 min did not worsen the gastric damage scores significantly (P greater than 0.1). In a third study, stimulation of both intact vagus nerves after paraventricular nucleus (PVN) lesion resulted in damage scores (0.33 +/- 0.17) that were significantly reduced compared with intact PVN and non-PVN-lesioned animals (P less than 0.01). These results indicate that the development of vagal stimulation-induced gastric damage requires the activation of both afferent and efferent vagal components and suggest further that such damage is dependent upon an intact PVN.
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Kentish, Stephen, Tracey A. O'Donnell, Gary Wittert, L. Ashley Blackshaw, and Amanda J. Page. "The “Leptin Switch” Mechanism in Gastric Vagal Afferents." Gastroenterology 140, no. 5 (May 2011): S—45. http://dx.doi.org/10.1016/s0016-5085(11)60180-7.
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Tougas, Gervais, and Lu Wang. "Pseudoaffective cardioautonomic responses to gastric distension in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 1 (July 1, 1999): R272—R278. http://dx.doi.org/10.1152/ajpregu.1999.277.1.r272.
Повний текст джерелаАнотація:
We examined the heart rate response to gastric distension, the involvement of vagal and sympathetic sensory afferents, adrenergic and cholinergic neural pathways, and the effects of capsaicin on this response in anesthetized rats. Gastric distension volume dependently decreased heart rate by 24.5% (resting rate = 219.87 ± 14.06 beats/min, mean rate during gastric distension with 15 ml = 165.97 ± 17.36 beats/min, P < 0.05). The bradycardic response was significantly decreased after removal of the celiac plexus (9.71 ± 1.77 vs. 38.03 ± 7.06% in controls, P < 0.05) or after bilateral subdiaphragmatic vagotomy (6.38 ± 2.65%, P = 0.05). The response to gastric distension was largely prevented by systemic capsaicin (29.92 ± 4.93% in controls, 2.58 ± 4.19% after systemic capsaicin, P < 0.05) and decreased by perivagal capsaicin (18.72 ± 4.75%, P < 0.05). Atropine almost completely prevented the cardiac response to distension, while propranolol and bretylium partially blocked it, implying the response is primarily mediated by cholinergic efferents but also involves adrenergic pathways. We conclude that unmyelinated, capsaicin-sensitive vagal afferents are essential to the pseudoaffective cardioautonomic response to a noxious gastric stimulus.
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Wang, Yu Hua, Yvette Taché, and Jen Yu Wei. "Cholecystokinin-responsive gastric vagal afferents in vitro in rats." Gastroenterology 114 (April 1998): A1189. http://dx.doi.org/10.1016/s0016-5085(98)84833-6.
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Teckentrup, Vanessa, Sandra Neubert, João C. P. Santiago, Manfred Hallschmid, Martin Walter, and Nils B. Kroemer. "Non-invasive stimulation of vagal afferents reduces gastric frequency." Brain Stimulation 13, no. 2 (March 2020): 470–73. http://dx.doi.org/10.1016/j.brs.2019.12.018.
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Ballsmider, L. A., A. C. Vaughn, M. David, A. Hajnal, P. M. Di Lorenzo, and K. Czaja. "Sleeve Gastrectomy and Roux-en-Y Gastric Bypass Alter the Gut-Brain Communication." Neural Plasticity 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/601985.
Повний текст джерелаАнотація:
This study investigated the anatomical integrity of vagal innervation of the gastrointestinal tract following vertical sleeve gastrectomy (VSG) and Roux-en-Y gastric bypass (RYGB) operations. The retrograde tracer fast blue (FB) was injected into the stomach to label vagal neurons originating from nodose ganglion (NG) and dorsal motor nucleus of the vagus (DMV). Microglia activation was determined by quantifying changes in the fluorescent staining of hindbrain sections against an ionizing calcium adapter binding molecule 1 (Iba1). Reorganization of vagal afferents in the hindbrain was studied by fluorescent staining against isolectin 4 (IB4). The density of Iba1- and IB4-immunoreactivity was analyzed using Nikon Elements software. There was no difference in the number of FB-labeled neurons located in NG and DMV between VSG and VSG-sham rats. RYGB, but not RYGB-sham rats, showed a dramatic reduction in number of FB-labeled neurons located in the NG and DMV. VSG increased, while the RYGB operation decreased, the density of vagal afferents in the nucleus tractus solitarius (NTS). The RYGB operation, but not the VSG procedure, significantly activated microglia in the NTS and DMV. Results of this study show that the RYGB, but not the VSG procedure, triggers microglia activation in vagal structures and remodels gut-brain communication.
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Kang, Y. M., K. Lamb, G. F. Gebhart, and K. Bielefeldt. "Experimentally induced ulcers and gastric sensory-motor function in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 2 (February 2005): G284—G291. http://dx.doi.org/10.1152/ajpgi.00250.2004.
Повний текст джерелаАнотація:
Prior studies have demonstrated that inflammation can sensitize visceral afferent neurons, contributing to the development of hyperalgesia. We hypothesized that both afferent and efferent pathways are affected, resulting in changes in motor and sensory function. Kissing ulcers (KU) were induced in the distal stomach by injecting 60% acetic acid for 45 s into a clamped area of the stomach. In controls, saline was injected into the stomach. A balloon catheter was surgically placed into the stomach, and electromyographic responses to gastric distension were recorded from the acromiotrapezius muscle at various times after ulcer induction. The accommodation reflex was assessed by slowly infusing saline into the distally occluded stomach. Gastric pressure changes in response to vagal stimulation were measured in anesthetized rats. Contractile function of circular muscle strips was examined in vitro using force-displacement transducers. KU caused gastric hypersensitivity that persisted for at least 14 days. Fluid distension of the stomach led to a rapid pressure increase in KU but not in control animals, consistent with an impaired accommodation reflex. Gastric ulcers enhanced the contractile response to vagal stimulation, whereas the effect of cholinergic stimulation on smooth muscle in vitro was not changed. These data suggest that inflammation directly alters gastric sensory and motor function. Increased activation of afferents will trigger vagovagal reflexes, thereby further changing motility and indirectly activating sensory neurons. Thus afferent and efferent pathways both contribute to the development of dyspeptic symptoms.
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Peters, J. H., B. M. McKay, S. M. Simasko, and R. C. Ritter. "Leptin-induced satiation mediated by abdominal vagal afferents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 4 (April 2005): R879—R884. http://dx.doi.org/10.1152/ajpregu.00716.2004.
Повний текст джерелаАнотація:
Leptin is a hormone secreted into the systemic blood primarily by white adipose tissue. However, leptin also is synthesized and stored by cells in the gastric mucosa. Because gastric mucosal leptin is secreted in response to ingestion of a meal, we hypothesized that it might contribute to satiation (meal termination) by acting on gastrointestinal vagal afferent neurons. To test whether leptin is capable of acutely reducing short-term food intake, we measured consumption of a liquid meal (15% sucrose) following low-dose leptin administration via the celiac artery, which perfuses the upper gastrointestinal tract. Leptin (1, 3, 10 μg) was infused via a chronically implanted, nonocclusive celiac arterial catheter or via a jugular vein catheter with its tip in the right cardiac atrium. Fifteen percent sucrose intake was then measured for 30 min. We found that leptin dose dependently inhibited sucrose intake when infused through the celiac catheter but not when infused into the general circulation via a jugular catheter. Plasma leptin concentrations in the general circulation following celiac arterial or jugular leptin infusions were not significantly different. Celiac arterial leptin infusion did not reduce meal size in vagotomized or capsaicin-treated rats. Finally, we also found that reduction of meal size by celiac leptin infusion was markedly enhanced when coinfused with cholecystokinin, a gastrointestinal satiety peptide whose action depends on vagal afferent neurons. Our results support the hypothesis that leptin contributes to satiation by a mechanism dependent on gastrointestinal vagal afferent innervation of the upper gastrointestinal tract.
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Berthoud, H. R., E. A. Fox, and T. L. Powley. "Localization of vagal preganglionics that stimulate insulin and glucagon secretion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 1 (January 1, 1990): R160—R168. http://dx.doi.org/10.1152/ajpregu.1990.258.1.r160.
Повний текст джерелаАнотація:
Although it is generally acknowledged that pancreatic islets are under powerful vagal control, specifics of vagal pathways and their central representation in the brain stem are unclear. To define this circuitry, we combined a protocol measuring electrical vagal stimulation-induced insulin and glucagon secretion with a retrograde tracer strategy that delineated the pool of spared motoneurons in the dorsal motor nucleus of the vagus (dmnX) following selective abdominal branch vagotomies. Three of the five branches mediated both insulin and glucagon release: posterior gastric (+198 and +117% increase from basal for insulin and glucagon, respectively), anterior gastric (+177 and +104%), and hepatic branch (+103 and +60%). In contrast, unreliable and nonsignificant hormonal responses were produced by stimulation of fibers projecting through either the posterior celiac (+12% insulin and +12% glucagon) or accessory celiac (+15% insulin and +31% glucagon) branches. Since hexamethonium almost completely blocked both insulin and glucagon responses to stimulation, the effects are not likely to have resulted from inadvertent antidromic excitation of vagal afferents. Cell bodies of stimulated motoneurons, which were responsible for insulin and glucagon secretion, were found to occupy the medial two-thirds of the right (projecting through the posterior gastric branch) and left (projecting through the anterior gastric and hepatic branches) dmnX. These medial, longitudinal dmnX columns and their associated abdominal vagal branches are likely to play the predominant role in vagal control of the endocrine pancreas.
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Holzer, H. H., C. M. Turkelson, T. E. Solomon, and H. E. Raybould. "Intestinal lipid inhibits gastric emptying via CCK and a vagal capsaicin-sensitive afferent pathway in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 4 (October 1, 1994): G625—G629. http://dx.doi.org/10.1152/ajpgi.1994.267.4.g625.
Повний текст джерелаАнотація:
The mechanism by which lipid in the duodenum inhibits gastric emptying was investigated in awake rats fitted with chronic gastric and duodenal cannulas. Perfusion of the duodenum with lipid (Intralipid, 5 and 10%; total amount 50 and 100 mg) caused a significant inhibition (26 and 78%, respectively) of gastric emptying of a nonnutrient liquid (0.9% saline). Functional ablation of the capsaicin-sensitive vagal, but not the spinal, sensory innervation to the upper gastrointestinal tract significantly attenuated by 57% lipid-induced inhibition of gastric emptying. In intact rats, administration of a specific cholecystokinin (CCK)-A receptor antagonist, devazepide, significantly attenuated by 66% the response to lipid. Administration of devazepide in perivagal capsaicin-treated rats did not further reduce the response to lipid. These results suggest that lipid in the duodenum inhibits gastric emptying via a mechanism involving an action of CCK at type A receptors and capsaicin-sensitive vagal afferents.
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Li, Hui, and Amanda J. Page. "Activation of CRF2 receptor increases gastric vagal afferent mechanosensitivity." Journal of Neurophysiology 122, no. 6 (December 1, 2019): 2636–42. http://dx.doi.org/10.1152/jn.00619.2019.
Повний текст джерелаАнотація:
Gastric vagal afferent (GVA) sensing of food-related mechanical stimuli is a crucial mechanism in the control of feeding behavior and gastric function. Stress is an important factor contributing to eating disorders and gastric diseases. Chronic stress has been shown to increase the mechanosensitivity of GVAs in mice and to reduce food intake and body weight. Whether the mechanosensitivity of GVAs is modulated by stress hormones is not known. This study aimed to determine the effect of stress hormones on GVA mechanosensitivity. The expression of stress hormone receptors in GVA cell bodies was determined in 8-wk-old male C57BL/6 mice using quantitative RT-PCR combined with laser capture microdissection. The mechanosensitivity of GVAs was determined in the absence and presence of stress hormones using an in vitro single-fiber recording preparation. NR3C1 and CRHR2 (mRNA isoforms of glucocorticoid receptor and CRF2 receptor, respectively) were expressed in GVA neurons. The glucocorticoid receptor agonist corticosterone had no effect on the mechanosensitivity of either tension or mucosal GVAs. Activation of CRF2 receptor by its specific analog, urocortin 3, significantly increased the mechanosensitivity of both tension and mucosal GVAs, an effect prevented by the CRF2 receptor antagonist astressin 2B. In conclusion, activation of CRF2 receptor increases the mechanosensitivity of GVAs. This may contribute to the stress- and CRF2 receptor-associated changes in feeding behavior and gastric function, possibly contributing to the hypersensitivity of GVAs in chronic stress conditions. NEW & NOTEWORTHY Gastric vagal afferents (GVAs) relay food-related signals to the central nervous system, where they are processed, eventually leading to modulation of food intake and gastric function. GVA signaling can be modulated by an array of hormones. Stress has been shown to induce GVA hypersensitivity. This study demonstrates that GVA neurons express subtypes of stress hormone receptors, specifically CRF2. Furthermore, activation of CRF2 receptor increases GVA mechanosensitivity, which could have implications for food intake and gastric function.
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Pittam, B. S., W. R. Ewart, F. Appia, and D. L. Wingate. "Physiological enteric stimulation elicits cardiovascular reflexes in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 3 (September 1, 1988): G319—G328. http://dx.doi.org/10.1152/ajpgi.1988.255.3.g319.
Повний текст джерелаАнотація:
By use of anesthetized rats, parameters for the activation of cardiovascular reflexes by stimulation of gastric or hepatic receptors have been established. For reflex activation, the mean minimum intragastric volume was 4 ml, and the mean minimum rate of hepatic portal vein infusion was 0.3 ml/min. Subdiaphragmatic vagotomy affected the response to gastric distension but did not appear to affect the response to hepatic portal vein infusion, indicating that vagal afferents are involved in mediating gastric-cardiovascular but not hepatic-cardiovascular reflexes. Experiments designed to emphasize the vagal component of the response to gastric distension confirmed this finding. Antagonist effects indicated that the tachycardia was mediated by beta-adrenoreceptor stimulation and that the pressor response was mainly mediated by alpha-adrenoreceptors. The data show that stimuli used in experiments to assess central processing of sensory information from the gastrointestinal tract can activate cardiovascular reflexes. Caution in the design of such experiments and in the interpretation of the data generated is indicated.
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Sharkey, Keith A., Lorraine D. Oland, David R. Kirk, and Joseph S. Davison. "Capsaicin-sensitive vagal stimulation-induced gastric acid secretion in the rat: evidence for cholinergic vagal afferents." British Journal of Pharmacology 103, no. 4 (August 1991): 1997–2003. http://dx.doi.org/10.1111/j.1476-5381.1991.tb12366.x.
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Barber, W. D., and T. F. Burks. "Brain-gut interactions: brain stem neuronal response to local gastric effects of substance P." American Journal of Physiology-Gastrointestinal and Liver Physiology 253, no. 3 (September 1, 1987): G369—G377. http://dx.doi.org/10.1152/ajpgi.1987.253.3.g369.
Повний текст джерелаАнотація:
Single-unit activity that responded to phasic gastric distension was recorded extracellularly from neurons in brain stem of anesthetized cats during local substance P chemically induced changes in wall tension. Local gastric intra-arterial administration of substance P via splenic artery often produced a triphasic gastric response. Gastric changes were characterized by 1) an initial brief increase in distension of corpus immediately after peptide and 2) a subsequent contraction that gave way to 3) a prolonged late increase in distension exceeding control levels. The contraction phase was atropine sensitive, suggesting that one mechanism of action during this phase was linked to cholinergic enteric nerves. Distension phases were unaffected by atropine, suggesting a different mechanism of action. Increase in gastric wall tension after peptide resulted in 1) onset of or enhanced activity of brain stem unit during nondistending phase and 2) greater spike discharge per unit change in volume during distending phase in many neurons. Some neurons showed a brief flurry of tonic activity during distending and nondistending phases of the cycle after local gastric injection of peptide with no observable change in wall tension. This suggests that the peptide may also act on chemoreceptors served by vagal primary afferents, which impinge on this neuronal population in the brain stem. Less than 10% of the neurons showed no change in discharge rate after a significant increase in wall tension, which occurred after local gastric injection of substance P, suggesting a mechanism of action involving input from primary vagal afferent fibers serving mucosal receptors unaffected by this level of change in wall tension.(ABSTRACT TRUNCATED AT 250 WORDS)
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Wei, Jen Yu, and Yu Hua Wang. "In vitro identification of corpus distension responsive gastric vagal afferents in rats." Gastroenterology 114 (April 1998): A1191. http://dx.doi.org/10.1016/s0016-5085(98)84838-5.
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Kiraly, A., G. Suto, E. H. Livingston, P. H. Guth, S. St Pierre, and Y. Tache. "Central vagal activation by TRH induces gastric hyperemia: role of CGRP in capsaicin-sensitive afferents in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 6 (December 1, 1994): G1041—G1049. http://dx.doi.org/10.1152/ajpgi.1994.267.6.g1041.
Повний текст джерелаАнотація:
The role of calcitonin gene-related peptide (CGRP) in the vagal cholinergic-mediated increase in gastric mucosal blood flow (GMBF) induced by the stable thyrotropin-releasing hormone (TRH) analogue RX-77368 injected intracisternally (ic, 30 ng) was investigated in urethan-anesthetized rats using the hydrogen gas clearance technique. alpha-CGRP (14 micrograms.kg-1.h-1) or bethanechol (150 micrograms.kg-1.h-1) infused close intra-arterially to the stomach or RX-77368 injected intracisternally increased GMBF by 76, 102, and 131%, respectively, 30 min after administration. The CGRP antagonist, human CGRP-(8-37) [hCGRP-(8-37)], injected intravenously (15 micrograms/kg bolus and 3 micrograms.kg-1.h-1) inhibited by 100, 97, and 73% the gastric hyperemic response to alpha-CGRP, TRH analogue, and bethanechol, respectively, whereas the substance P antagonist CP-96,345 (3 mg/kg iv) had no effect. In capsaicin-pretreated rats, hCGRP-(8-37) no longer blocked the increase in GMBF induced by intracisternal RX-77368. These results suggest that the gastric hyperemic response to central vagal activation induced by intracisternal TRH analogue at 30 ng is mediated by local effector function of capsaicin-sensitive afferent fibers releasing CGRP.
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Mönnikes, Hubert, Gerd Lauer, Christoph Bauer, Johannes Tebbe, Tillmann T. Zittel, and Rudolf Arnold. "Pathways of Fos expression in locus ceruleus, dorsal vagal complex, and PVN in response to intestinal lipid." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 6 (December 1, 1997): R2059—R2071. http://dx.doi.org/10.1152/ajpregu.1997.273.6.r2059.
Повний текст джерелаАнотація:
Exogenous cholecystokinin (CCK) injected peripherally mimics effects of lipid entering the intestine on food intake and gastric motility via vagal afferents and induces c- fos expression in the locus ceruleus complex (LCC), nucleus of the solitary tract (NTS), area postrema (AP), and paraventricular nucleus (PVN). However, the role of peripheral endogenous CCK in induction of c- fos expression in the brain at ingestion of nutrients is controversial. In awake rats, intraduodenal lipid infusion markedly increased Fos protein-like immunoreactivity (FLI) in these brain nuclei. Perivagal capsaicin pretreatment reduced the increase of FLI in the LCC, NTS, and PVN by 66–86% and in the AP by 46%. The CCK-A receptor antagonist MK-329 (0.1 mg/kg ip) diminished the FLI increase in LC, NTS, AP, and PVN by 39–100%; the CCK-B receptor antagonist L-365,260 reduced the increased FLI in the AP by 54%. After capsaicin pretreatment, both CCK antagonists had additional inhibitory effects only on FLI in the AP. These findings suggest that entry of lipid into the intestine activates c- fos in the LCC, NTS, and PVN predominantly via CCK-A receptors on vagal afferents and in the AP via vagal and nonvagal pathways, as well as CCK-B and CCK-A receptors.
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Page, Amanda J. "Gastrointestinal Vagal Afferents and Food Intake: Relevance of Circadian Rhythms." Nutrients 13, no. 3 (March 5, 2021): 844. http://dx.doi.org/10.3390/nu13030844.
Повний текст джерелаАнотація:
Gastrointestinal vagal afferents (VAs) play an important role in food intake regulation, providing the brain with information on the amount and nutrient composition of a meal. This is processed, eventually leading to meal termination. The response of gastric VAs, to food-related stimuli, is under circadian control and fluctuates depending on the time of day. These rhythms are highly correlated with meal size, with a nadir in VA sensitivity and increase in meal size during the dark phase and a peak in sensitivity and decrease in meal size during the light phase in mice. These rhythms are disrupted in diet-induced obesity and simulated shift work conditions and associated with disrupted food intake patterns. In diet-induced obesity the dampened responses during the light phase are not simply reversed by reverting back to a normal diet. However, time restricted feeding prevents loss of diurnal rhythms in VA signalling in high fat diet-fed mice and, therefore, provides a potential strategy to reset diurnal rhythms in VA signalling to a pre-obese phenotype. This review discusses the role of the circadian system in the regulation of gastrointestinal VA signals and the impact of factors, such as diet-induced obesity and shift work, on these rhythms.
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Nosaka, S., S. Murase, and K. Murata. "Arterial baroreflex inhibition by gastric distension in rats: mediation by splanchnic afferents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 5 (May 1, 1991): R985—R994. http://dx.doi.org/10.1152/ajpregu.1991.260.5.r985.
Повний текст джерелаАнотація:
Arterial baroreflexes are known to be reset during activation of defense area and somatosensory receptors-afferents. Here we report that viscerosensory activation also inhibits the baroreflexes. In chloralose-urethan-anesthetized, succinylcholine-immobilized, and artificially ventilated rats, the aortic depressor nerve was electrically stimulated while propranolol was continuously infused to elicit baroreflex hypotension (BH) and baroreflex vagal bradycardia (BVB). Hydraulic distension of the stomach with warm 0.9% NaCl solution was found to suppress BVB and BH, with a threshold intraluminal pressure at times less than 5mmHg. The gastric distension also suppressed BH in atropinized rats, suggesting that inhibition involved not only cardiac but also vascular components of baroreflexes. Bilateral splanchnectomy largely attenuated the inhibition, whereas bilateral subdiaphragmatic vagotomy had little effect. Low- as well as high-frequency stimulation of the splanchnic nerve strongly suppressed both BVB and BH, whereas only low-frequency stimulation of the subdiaphragmatic vagus inhibited baroreflexes to a slight degree. In conclusion, gastric distension suppresses BVB and BH, and this inhibition is largely mediated by afferent fibers in the splanchnic nerve. Such baroreflex inhibition may be a general consequence of mechanoreceptor activation of any visceral hollow organs because the jejunum, esophagus, and urinary bladder were all found to suppress arterial baroreflexes when distended.
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Kaneko, Hiroshi, Jonathan Kaunitz, and Yvette Taché. "Vagal mechanisms underlying gastric protection induced by chemical activation of raphe pallidus in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 5 (November 1, 1998): G1056—G1062. http://dx.doi.org/10.1152/ajpgi.1998.275.5.g1056.
Повний текст джерелаАнотація:
Peripheral mechanisms involved in kainic acid injected into the raphe pallidus (Rpa)-induced gastric protection were investigated in urethan-anesthetized rats. Gastric mucosal blood flow (GMBF), acid secretion, and gastric injury induced by intragastric ethanol (60%) were measured in response to kainic acid (25 pg) injected into the Rpa. Kainic acid reduced ethanol-induced gastric lesions by 57%. The protective effect was blocked by vagotomy, capsaicin deafferentation, and intravenous injection of the calcitonin gene-related peptide (CGRP) antagonist CGRP-(8—37) and NG-nitro-l-arginine methyl ester (l-NAME).l- but notd-arginine reversed thel-NAME action. Kainic acid injected into the Rpa, unlike outside sites, increased basal GMBF but not acid secretion. Indomethacin unmasked an acid secretory response to kainic acid. These results show that kainic acid injected into the Rpa at a dose that did not stimulate acid secretion, due to the inhibitory effect of prostaglandins, protects against ethanol-induced gastric injury through vagal-dependent activation of CGRP contained in capsaicin-sensitive afferents and nitric oxide-mediated gastric vasodilatory mechanisms.
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Talman, W. T., K. Andreasen, J. Calvin, and S. Eversmann-Johanns. "Cholecystokinin in nucleus tractus solitarii modulates tonic and phasic gastric pressure." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 1 (July 1, 1991): R217—R222. http://dx.doi.org/10.1152/ajpregu.1991.261.1.r217.
Повний текст джерелаАнотація:
Local excitation of neurons at the site of termination of gastric vagal afferents in the nucleus tractus solitarii (NTS) alters gastric pressure. Microinjection of one putative satiety peptide bombesin into NTS increases pressure while substance P lowers it. Therefore, we sought to determine the effects of the microinjection of cholecystokinin octapeptide (CCK-8) from micropipettes placed stereotactically into the NTS of anesthetized rats with balloons placed in the gastric antrum to sense gastric pressure waves. Sulfated CCK-8, but not nonsulfated CCK-8, produced dose-dependent decreases of gastric pressure, transient blockade of phasic waves, and subsequent dysrhythmic phasic activity. The effects were specifically related to injections into NTS and did not occur with injections given intravenously, intracisternally, or into tissue adjacent to NTS. These results support a role for CCK-8 in central regulation of not only tonic gastric pressure but also phasic activity and gastric motility.
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Furukawa, Naohiro, Mizue Hatano, and Hiroyuki Fukuda. "Glutaminergic vagal afferents may mediate both retching and gastric adaptive relaxation in dogs." Autonomic Neuroscience 93, no. 1-2 (October 2001): 21–30. http://dx.doi.org/10.1016/s1566-0702(01)00322-8.
Повний текст джерела
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Malbert, Charles-Henri. "Vagally Mediated Gut-Brain Relationships in Appetite Control-Insights from Porcine Studies." Nutrients 13, no. 2 (January 30, 2021): 467. http://dx.doi.org/10.3390/nu13020467.
Повний текст джерелаАнотація:
Signals arising from the upper part of the gut are essential for the regulation of food intake, particularly satiation. This information is supplied to the brain partly by vagal nervous afferents. The porcine model, because of its sizeable gyrencephalic brain, omnivorous regimen, and comparative anatomy of the proximal part of the gut to that of humans, has provided several important insights relating to the relevance of vagally mediated gut-brain relationships to the regulation of food intake. Furthermore, its large size combined with the capacity to become obese while overeating a western diet makes it a pivotal addition to existing murine models, especially for translational studies relating to obesity. How gastric, proximal intestinal, and portal information relating to meal arrival and transit are encoded by vagal afferents and their further processing by primary and secondary brain projections are reviewed. Their peripheral and central plasticities in the context of obesity are emphasized. We also present recent insights derived from chronic stimulation of the abdominal vagi with specific reference to the modulation of mesolimbic structures and their role in the restoration of insulin sensitivity in the obese miniature pig model.
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Wei, Jen Yu, and Yu Hua Wang. "Effect of CCK pretreatment on the CCK sensitivity of rat polymodal gastric vagal afferent in vitro." American Journal of Physiology-Endocrinology and Metabolism 279, no. 3 (September 1, 2000): E695—E706. http://dx.doi.org/10.1152/ajpendo.2000.279.3.e695.
Повний текст джерелаАнотація:
To prevent the blood-borne interference and reflex actions via neighboring organs and the central nervous system, the study was conducted in an in vitro isolated stomach-gastric vagus nerve preparation obtained from overnight-fasted, urethan-anesthetized rats. Afferent unit action potentials were recorded from the gastric branch of the vagus nerve. The left gastric artery was catheterized for intra-arterial injection. In vitro we found that 1) 55/70 gastric vagal afferents (GVAs) were polymodal, responding to CCK-8 and mechanical stimuli, 13 were mechanoreceptive, and 2 were CCK-responsive; 2) sequential or randomized intra-arterial injections of CCK-8 (0.1–200 pmol) dose-dependently increased firing rate and reached the peak rate at 100 pmol; 3) the action was suppressed by CCK-A (Devazepide) but not by CCK-B (L-365,260) receptor antagonist; 4) neither antagonist blocked the mechanosensitivity of GVA fibers. These results are consistent with corresponding in vivo well-documented findings. Histological data indicate that the layered structure of the stomach wall was preserved in vitro for 6–8 h. Based on these results, it seems reasonable to use the in vitro preparation for conducting a study that is usually difficult to be performed in vivo. For instance, because there was no blood supply in vitro, the composition of the interstitial fluid, i.e., the ambient nerve terminals, can be better controlled and influenced by intra-arterial injection of a defined solution. Here we report that acutely changing the ambient CCK level by a conditioning stimulus (a preceding intra-arterial injection of increasing doses of CCK-8) reduced the CCK sensitivity of GVA terminals to a subsequent test stimulus (a constant dose of CCK-8 intra-arterial injection).
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Cuche, G., S. Blat, and C. H. Malbert. "Desensitization of ileal vagal receptors by short-chain fatty acids in pigs." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 5 (May 1, 2001): G1013—G1021. http://dx.doi.org/10.1152/ajpgi.2001.280.5.g1013.
Повний текст джерелаАнотація:
Coloileal reflux episodes trigger specialized ileal motor activities and inhibit gastric motility in pigs. The initiation of these events requires the detection by the distal ileum of the invading colonic contents that differ from the ileal chyme primarily in short-chain fatty acid (SCFA) concentrations. In addition to the already described humoral pathway, this detection might also involve ileal vagal afferents. Sensitivity to SCFA of 12 ileal vagal units was investigated in anesthetized pigs with single-unit recording at the left cervical vagus. SCFA mixtures (0.35, 0.7, and 1.4 mol/l) containing acetic, propionic, and butyric acids in proportions identical to that in the porcine cecocolon were compared with isotonic and hypertonic saline. All units behaved as slowly adapting mechanoreceptors (half-adaptation time = 35.4 ± 15.89 s), and their sensitivity to local mechanical probing was suppressed by local anesthesia; 7 units significantly decreased their spontaneous firing with 0.7 and 1.4 but not 0.35 mol/l SCFA infusion compared with hypertonic or isotonic saline. Similarly, the response induced by distension in the same seven units was reduced (5 neurons) or abolished (2 neurons) after infusion of 0.7 (22.8 ± 2.39 impulses/s) and 1.4 (30.3 ± 2.12 impulses/s) mol/l SCFA solutions compared with isotonic saline (38.6 ± 4.09 impulses/s). These differences in discharge were not the result of changes in ileal compliance, which remained constant after SCFA. In conclusion, SCFA, at concentrations near those found during coloileal reflux episodes, reduced or abolished mechanical sensitivity of ileal vagal afferents.
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Wang, Y. H., Y. Tache, A. B. Sheibel, V. L. Go, and J. Y. Wei. "Two types of leptin-responsive gastric vagal afferent terminals: an in vitro single-unit study in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 2 (August 1, 1997): R833—R837. http://dx.doi.org/10.1152/ajpregu.1997.273.2.r833.
Повний текст джерелаАнотація:
In vitro gastric vagal afferents' (GVAs) unit activities were recorded from the ventral GVA nerve strands in rats. The responsiveness of 16 GVA terminals to close intra-arterial injection of vehicle (0.1 ml), leptin (350 pmol), and cholecystokinin (CCK)-8 (10 pmol) was analyzed to generate a spike count-versus-time histogram. Data of 5-min spike counts before and after each treatment were normalized by dividing the latter by the former. A quotient (Q) > 1 indicates an excitatory effect, Q < 1 indicates an inhibitory effect, and Q close to 1 indicates no effect. Two types of GVA terminals were identified. Type 1 (n = 8) responded to leptin with Q > 1; CCK-8 pretreatment did not consistently alter leptin sensitivity. In contrast, Type 2 (n = 8) responded to leptin with Q < 1 or close to 1, and CCK-8 pretreatment increased the leptin sensitivity so that the terminals responded to subsequent leptin with Q > 1. These data suggest that Type 1 and Type 2 GVA terminals may provide afferent neural signals, which, in turn, will be involved in body weight and food intake control systems, respectively.
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Willing, A. E., and H. R. Berthoud. "Gastric distension-induced c-fos expression in catecholaminergic neurons of rat dorsal vagal complex." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 1 (January 1, 1997): R59—R67. http://dx.doi.org/10.1152/ajpregu.1997.272.1.r59.
Повний текст джерелаАнотація:
Functionally specific vagal afferents were stimulated by gastric balloon distension in unanesthetized rats, followed by double c-fos/dopamine beta-hydroxylase (DBH) immunocytochemistry, to identify second-order neurons in the dorsal vagal complex. Continuous and repeated phasic distension with similar volumes produced similar numbers and patterns of c-fos expression, with most of the activated neurons in the medial and commissural nucleus of the solitary tract (NTS) and dorsal motor nucleus (DMNX). Larger distension activated significantly more neurons in all responsive areas but there was no differential effect. In most NTS subnuclei and the DMNX, a small (3-5%) proportion of gastric distension-activated neurons was DBH-immunoreactive (DBH-IR), and this proportion did not significantly change with type of distension. With continuous and repeated small distensions, 10-12% and, with the large distension, 22-30% of all DBH-IR neurons expressed c-fos. The results suggest a large degree of convergence between rapidly adapting mucosal receptors and slowly adapting tension receptors, but not between low- and high-threshold tension receptors, and a relatively minor role of catecholaminergic second-order neurons in the dissemination of distension signals in the brain.