scholarly journals The role of non-myelinated vagal afferent fibres from the lungs in the genesis of tachypnoea in the rabbit

1971 ◽  
Vol 213 (2) ◽  
pp. 345-371 ◽  
Author(s):  
A. Guz ◽  
Diana W. Trenchard
Keyword(s):  
Author(s):  
Marian Kollarik ◽  
Fei Ru ◽  
Nikoleta Pavelkova ◽  
John Mulcahy ◽  
John Hunter ◽  
...  

2007 ◽  
Vol 293 (2) ◽  
pp. R635-R641 ◽  
Author(s):  
Maria A. Zafra ◽  
Filomena Molina ◽  
Amadeo Puerto

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.


1972 ◽  
Vol 42 (3) ◽  
pp. 251-263 ◽  
Author(s):  
Diana Trenchard ◽  
D. Gardner ◽  
A. Guz

1. The administration of the polysaccharide carageenin through a catheter into the lungs of cats and rabbits has produced an inflammatory lesion confined to one lobe of a lung. The lesion consisted of an alveolar and interstitial infiltration with polymorphonuclear leucocytes and, subsequently, macrophages. There was no apparent damage to alveolar walls and no pleurisy. The rest of the lung remained normal. 2. In both conscious cats and anaesthetized rabbits there was an increased frequency of breathing dependent on an intact vagus nerve on the same side as the lesion. It was independent of changes in body temperature and was not due to hypoxaemia. 3. By using a direct current to the right cervical vagus nerve in the rabbits (with the left vagus nerve sectioned), it has been possible to block conduction in myelinated fibres; the non-myelinated fibres conduct normally. Studies with this differentially blocked nerve have shown that the increased frequency of breathing is dependent on activity in the non-myelinated vagal afferent fibres.


Endocrinology ◽  
2005 ◽  
Vol 146 (5) ◽  
pp. 2369-2375 ◽  
Author(s):  
Shuichi Koda ◽  
Yukari Date ◽  
Noboru Murakami ◽  
Takuya Shimbara ◽  
Takeshi Hanada ◽  
...  

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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