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.

Subdiaphragmatic vagal deafferentation fails to block feeding-suppressive effects of LPS and IL-1 beta in rats

1997 ◽  
Vol 273 (3) ◽  
pp. R1193-R1198 ◽  
Author(s):  
G. J. Schwartz ◽  
C. R. Plata-Salaman ◽  
W. Langhans
Keyword(s):  
Food Intake ◽  
Interleukin 1 ◽  
Glucose Consumption ◽  
Vagal Afferents ◽  
Afferent Pathways ◽  
Afferent Fibers ◽  
Inhibit Food Intake ◽  
Vagal Afferent ◽  
Left Vagus

To evaluate the role of subdiaphragmatic vagal afferent fibers in mediating the inhibition of food intake produced by peripheral administration of bacterial lipopolysaccharide (LPS) and the proinflammatory cytokine interleukin-1 beta (IL-1 beta), we assessed the ability of 100 micrograms/kg ip LPS and 2 micrograms/kg ip human recombinant IL-1 beta to suppress solid food intake during the first 3 and 6 h of the dark cycle in rats with selective vagal rootlet deafferentation (SDA, n = 15) and in sham surgical control rats (Con, n = 17). SDA was produced by a combination of dorsal subdiaphragmatic truncal vagotomy and left vagal afferent rootlet transection as the left vagus enters the caudal brain stem. Both LPS and IL-1 beta significantly suppressed food intake at 3 and 6 h in both Con and SDA rats, and SDA failed to attenuate the LPS- and IL-1 beta-induced reductions in food consumption relative to the suppression seen in controls. Peripheral administration of the gut-brain peptide cholecystokinin (CCK) suppressed 30-min 12.5% liquid glucose consumption in control, but not in SDA rats, consistent with previous demonstrations of the role of subdiaphragmatic vagal afferents in the mediation of CCK satiety. These data demonstrate that subdiaphragmatic vagal afferents are not necessary for the feeding-suppressive actions of peripherally administered LPS and IL-1 beta and suggest that peripheral LPS and IL-1 beta may inhibit food intake via humoral and/or splanchnic visceral afferent pathways.

Subdiaphragmatic vagotomy blocks induction of IL-1 beta mRNA in mice brain in response to peripheral LPS

1995 ◽  
Vol 268 (5) ◽  
pp. R1327-R1331 ◽  
Author(s):  
S. Laye ◽  
R. M. Bluthe ◽  
S. Kent ◽  
C. Combe ◽  
C. Medina ◽  
...  
Keyword(s):  
Immune System ◽  
Physiological Saline ◽  
General Activity ◽  
Chain Reaction ◽  
Afferent Fibers ◽  
Brain Expression ◽  
Mice Brain ◽  
Polymerase Chain ◽  
Vagal Afferent ◽  
The Brain

To test the possibility that the vagus nerve is involved in the communication between the immune system and the brain, we injected sham-operated and vagotomized mice with physiological saline or lipopolysaccharide (LPS; 400 micrograms/kg ip). Vagotomy attenuated LPS-induced depression of general activity measured 2 h after treatment but did not alter the increase in plasma levels of IL-1 beta in response to LPS. In addition, vagotomy abrogated the LPS-induced increase in the levels of transcripts for IL-1 beta, as determined by semiquantitative polymerase chain reaction after reverse transcription, in the hypothalamus and hippocampus, but not in the pituitary of vagotomized mice. This relationship between the effects of vagotomy on the behavioral effects of LPS and the LPS-induced brain expression of IL-1 beta mRNA indicates that vagal afferent fibers play a prominent role in the pathways of communication between the immune system and the brain.

scholarly journals The Role of the Vagal Nerve in Peripheral PYY3–36-Induced Feeding Reduction in Rats

Endocrinology ◽  
2005 ◽  
Vol 146 (5) ◽  
pp. 2369-2375 ◽  
Author(s):  
Shuichi Koda ◽  
Yukari Date ◽  
Noboru Murakami ◽  
Takuya Shimbara ◽  
Takeshi Hanada ◽  
...  
Keyword(s):  
Peptide Yy ◽  
Gastrointestinal Hormones ◽  
Blood Stream ◽  
Afferent Nerve ◽  
Solitary Tract ◽  
Afferent Fibers ◽  
Vagal Afferent ◽  
Glucagon Like Peptide 1 ◽  
The Brain

Abstract Peptide YY (PYY), an anorectic peptide, is secreted postprandially from the distal gastrointestinal tract. PYY3–36, the major form of circulating PYY, binds to the hypothalamic neuropeptide Y Y2 receptor (Y2-R) with a high-affinity, reducing food intake in rodents and humans. Additional gastrointestinal hormones involved in feeding, including cholecystokinin, glucagon-like peptide 1, and ghrelin, transmit satiety or hunger signals to the brain via the vagal afferent nerve and/or the blood stream. Here we determined the role of the afferent vagus nerve in PYY function. Abdominal vagotomy abolished the anorectic effect of PYY3–36 in rats. Peripheral administration of PYY3–36 induced Fos expression in the arcuate nucleus of sham-operated rats but not vagotomized rats. We showed that Y2-R is synthesized in the rat nodose ganglion and transported to the vagal afferent terminals. PYY3–36 stimulated firing of the gastric vagal afferent nerve when administered iv. Considering that Y2-R is present in the vagal afferent fibers, PYY3–36 could directly alter the firing rate of the vagal afferent nerve via Y2-R. We also investigated the effect of ascending fibers from the nucleus of the solitary tract on the transmission of PYY3–36-mediated satiety signals. In rats, bilateral midbrain transections rostral to the nucleus of the solitary tract also abolished PYY3–36-induced reductions in feeding. This study indicates that peripheral PYY3–36 may transmit satiety signals to the brain in part via the vagal afferent pathway.

Anti-inflammatory effects of leptin and cholecystokinin on acetic acid-induced colitis in rats: role of capsaicin-sensitive vagal afferent fibers

2003 ◽  
Vol 116 (1-3) ◽  
pp. 109-118 ◽  
Author(s):  
Ayhan Bozkurt ◽  
Barış Çakır ◽  
Feriha Ercan ◽  
Berrak Ç. Yeğen
Keyword(s):  
Acetic Acid ◽  
Afferent Fibers ◽  
Vagal Afferent ◽  
Anti Inflammatory

Conditioned flavor preference learning by intragastric administration of l-glutamate in rats

2009 ◽  
Vol 451 (3) ◽  
pp. 190-193 ◽  
Author(s):  
Akira Uematsu ◽  
Tomokazu Tsurugizawa ◽  
Takashi Kondoh ◽  
Kunio Torii
Keyword(s):  
Preference Learning ◽  
Intragastric Administration ◽  
Flavor Preference ◽  
Conditioned Flavor

Rapid, shallow breathing after Ascaris suum antigen inhalation: role of vagus nerves

1977 ◽  
Vol 42 (1) ◽  
pp. 101-106 ◽  
Author(s):  
D. J. Cotton ◽  
E. R. Bleecker ◽  
S. P. Fischer ◽  
P. D. Graf ◽  
W. M. Gold ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Ascaris Suum ◽  
Minute Volume ◽  
Vagus Nerves ◽  
Pulmonary Resistance ◽  
Afferent Pathways ◽  
Airway Narrowing ◽  
Shallow Breathing ◽  
Vagal Afferent

In five treadmill-exercising, unsedated dogs, we studied the effect of inhaled Ascaris suum antigen aerosols on minute volume of ventilation (VE), respiratory frequency (f), tidal volume (VT), total pulmonary resistance (RL), and dynamic pulmonary compliance (CLdyn), before and during cooling of the vagus nerves. With the vagi warm, inhaled antigen increased VE (mean + 62%; P less than 0.01)by increasing f (mean + 180%; P less than 0.01), despite a decrease in VT (mean - 42%; P less than 0.01). RL increased (mean + 170%; P less than 0.001) and CLdyn decreased (mean - 43%; P less than 0.005). With the vagi cool, inhaled antigen no longer affected VE, f, or VT (P greater than 0.5), although RL still increased and CLdyn still decreased. Inhalation of a bronchodilator, terbutaline, prevented the broncho-constriction induced by antigen but did not prevent the ventilatory response. We conclude that vagal afferent pathways mediate the ventilatory response to inhaled antigen and suggest that the primary stimulus for this response is not airway narrowing.

Secretin activates vagal primary afferent neurons in the rat: evidence from electrophysiological and immunohistochemical studies

2005 ◽  
Vol 289 (4) ◽  
pp. G745-G752 ◽  
Author(s):  
Ying Li ◽  
Xiaoyin Wu ◽  
Harry Yao ◽  
Chung Owyang
Keyword(s):  
Sensory Neurons ◽  
Neuronal Response ◽  
Afferent Pathways ◽  
Nodose Ganglia ◽  
Afferent Fibers ◽  
Intestinal Distension ◽  
Vagal Afferent ◽  
Immunohistochemical Studies ◽  
Afferent Response ◽  
First Time

In this study, we evaluated the vagal afferent response to secretin at physiological concentrations and localized the site of secretin's action on vagal afferent pathways in the rat. The discharge of sensory neurons supplying the gastrointestinal tract was recorded from nodose ganglia. Of 91 neurons activated by electrical vagal stimulation, 19 neurons showed an increase in firing rate in response to intestinal perfusion of 5-HT (from 1.5 ± 0.2 to 25 ± 4 impulses/20 s) but no response to intestinal distension. A close intra-arterial injection of secretin (2.5 and 5.0 pmol) elicited responses in 15 of these 19 neurons (from 1.5 ± 0.2 impulses/20 s at basal to 21 ± 4 and 43 ± 5 impulses/20 s, respectively). Subdiaphragmatic vagotomy and perivagal application of capsaicin, but not supranodose vagotomy, completely abolished the secretin-elicited vagal nodose neuronal response. In a separate study, 9 tension receptor afferents among 91 neurons responded positively to intestinal distension but failed to respond to luminal 5-HT. These nine neurons also showed no response to administration of secretin. As expected, immunohistochemical studies showed that secretin administration significantly increased the number of Fos-positive neurons in vagal nodose ganglia. In conclusion, we demonstrated for the first time that vagal sensory neurons are activated by secretin at physiological concentrations. A subpopulation of secretin-sensitive vagal afferent fibers is located in the intestinal mucosa, many of which are responsive to luminal 5-HT.

Cholecystokinin inhibits gastric motility and emptying via a capsaicin-sensitive vagal pathway in rats

1988 ◽  
Vol 255 (2) ◽  
pp. G242-G246 ◽  
Author(s):  
H. E. Raybould ◽  
Y. Tache
Keyword(s):  
Gastric Emptying ◽  
Gastric Motility ◽  
Physiological Role ◽  
Intragastric Administration ◽  
Liquid Meal ◽  
C Fibers ◽  
Afferent Fibers ◽  
Mesenteric Ganglion ◽  
Vagal Afferent ◽  
Celiac Ganglionectomy

The pathway by which cholecystokinin octapeptide (CCK-8) inhibits motility of the proximal stomach and the role of this pathway in the CCK-induced delay in gastric emptying of a liquid meal has been studied in rats by selective destruction of vagal afferent C-fibers using bilateral perineural application of the sensory neurotoxin, capsaicin, 3 or 4 days prior to the experiment. The capsaicin treatment significantly attenuated the decrease in intragastric pressure in urethan-anesthetized rats in response to CCK-8 (0.1-100 pmol iv) compared with vehicle-treated controls. Removal of the celiac-superior mesenteric ganglion completely abolished the inhibitory action of CCK-8 on gastric motility in these rats. In contrast, only celiac ganglionectomy in combination with vagotomy abolished the CCK-8 effect in vehicle-treated controls. Intravenous injection of CCK-8 (300 pmol) 5 min before intragastric administration of a methylcellulose solution decreased gastric emptying by 55% in conscious control or vehicle-treated rats. Perivagal capsaicin treatment abolished the delay in gastric emptying induced by CCK-8. In addition, capsaicin treatment alone significantly increased gastric emptying. These results demonstrate that CCK-8 decreases gastric motility in the gastric corpus and delays gastric emptying by a capsaicin-sensitive vagal afferent pathway. These same afferent fibers may also play a physiological role in the gastric emptying of liquids.

1245: Role of C-Afferent Fibers and Monitoring of Intra Vesical Resiniferatoxin Therapy for Patients with Idiopathic Detrusor Overactivity

2004 ◽  
Vol 171 (4S) ◽  
pp. 328-328
Author(s):  
Teruhiko Yokoyama ◽  
Kunihiro Nozaki ◽  
Osamu Fujita ◽  
Miyabi Inoue ◽  
Hiromi Kumon
Keyword(s):  
Detrusor Overactivity ◽  
Idiopathic Detrusor Overactivity ◽  
Afferent Fibers
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