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

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.

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Substantial role of locus coeruleus-noradrenergic activation and capsaicin-insensitive primary afferent fibers in bee venom's anti-inflammatory effect

Neuroscience Research ◽

10.1016/j.neures.2006.03.003 ◽

2006 ◽

Vol 55 (2) ◽

pp. 197-203 ◽

Cited By ~ 22

Author(s):

Young Bae Kwon ◽

Seo Yeon Yoon ◽

Hyun Woo Kim ◽

Dae Hyun Roh ◽

Seuk Yun Kang ◽

...

Keyword(s):

Locus Coeruleus ◽

Primary Afferent ◽

Substantial Role ◽

Afferent Fibers ◽

Primary Afferent Fibers ◽

Anti Inflammatory ◽

Inflammatory Effect

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

Endocrinology ◽

10.1210/en.2004-1266 ◽

2005 ◽

Vol 146 (5) ◽

pp. 2369-2375 ◽

Cited By ~ 272

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.

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Possible role of adrenergic mechanisms in the systemic anti-inflammatory activity of acetic acid in rats

European Journal of Pharmacology ◽

10.1016/0014-2999(74)90222-2 ◽

1974 ◽

Vol 26 (2) ◽

pp. 158-165 ◽

Cited By ~ 5

Author(s):

D.C. Atkinson ◽

R. Hicks

Keyword(s):

Acetic Acid ◽

Inflammatory Activity ◽

Adrenergic Mechanisms ◽

Anti Inflammatory

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Afferent Fibers of the Hypogastric Nerves Are Involved in the Facilitating Effects of Chemical Bladder Irritation in Rats

Journal of Neurophysiology ◽

10.1152/jn.2001.86.5.2276 ◽

2001 ◽

Vol 86 (5) ◽

pp. 2276-2284 ◽

Cited By ~ 49

Author(s):

Takahiko Mitsui ◽

Hidehiro Kakizaki ◽

Shinobu Matsuura ◽

Kaname Ameda ◽

Mitsuhiro Yoshioka ◽

...

Keyword(s):

Spinal Cord ◽

Acetic Acid ◽

Marked Decrease ◽

Lumbar Spinal Cord ◽

Urinary Frequency ◽

Acid Infusion ◽

Afferent Fibers ◽

Fos Expression ◽

Lumbar Spinal

To evaluate the role of bladder afferent fibers in the hypogastric nerves (HGN) in modulation of the micturition reflex induced by chemical bladder irritation, voiding behavior, continuous cystometry, and spinal c-fos expression following intravesical acetic acid instillation were investigated in rats with or without HGN transection. Voiding behavior and continuous cystometry were examined in unanesthetized conscious rats. Following chemical bladder irritation, a significant increase in urinary frequency associated with a marked decrease in the voided volume per micturition, was noted in control rats with the intact HGN, but not in HGN-transected rats. Continuous infusion of acetic acid in control rats elicited irritative bladder responses characterized by a marked decrease in the intercontraction interval and a marked increase in maximal vesical pressure, both of which were absent in capsaicin-desensitized rats. HGN transection prevented the decrease in the intercontraction interval but not an increase in maximal vesical pressure following chemical bladder irritation. Compared with saline infusion, acetic acid infusion caused a significant increase in c-fos expression at L1 and L6 of the spinal cord, and HGN transection significantly reduced c-fos expression in the dorsal horn of the spinal cord at L1 but not at L6. These results suggest that capsaicin-sensitive bladder afferent fibers in the HGN, which travel through the rostral lumbar spinal cord, have a role in urinary frequency caused by chemical bladder irritation.

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

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.273.3.r1193 ◽

1997 ◽

Vol 273 (3) ◽

pp. R1193-R1198 ◽

Cited By ~ 12

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.

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