The fiber composition of the abdominal vagus of the rat

Abstract

The present study provides a LM and EM inventory of the fibers of the rat abdominal vagus, including dorsal and ventral trunks and the five primary branches. Whole mounts (n = 15) were prepared to characterize the branching patterns. A set of EM samples consisting of both trunks and all branches (i.e. dorsal and ventral gastric, dorsal and accessory celiac, and hepatic) were then obtained from each of six additional animals. A complete cross-sectional montage (x 10000) was prepared from each sample. All axons were counted, and greater than 10% of them were evaluated morphometrically. The means of unmyelinated axon diameters for each of the five branches were similar (0.75-0.83 microns). However, the shapes of the fiber size distributions, as summarized by their skew coefficients, revealed that the two gastric branches differed significantly from the two celiac branches; furthermore, the hepatic size distribution differed from all others. Most of the myelinated fibers (85%) in all branches were less than 2.6 microns in diameter and had sheath widths between 0.1 and 0.5 micron. The gastric branches, however, also contained a few larger myelinated fibers with sheath widths as great as 0.85 micron. Whole mounts revealed fibers which were not of supradiaphragmatic origin within all five vagal branches; these adventitial bundles were traced along the perineurium between adjacent branches. The sum of the fibers in the five branches (26930) was 21% more than the number counted in the parent trunks (22272); this excess probably reflects the adventitial fiber content. The whole mounts also showed that a large and regularly positioned paraganglion was associated with the dorsal branches. The structural profiles observed (i.e. unmyelinated and myelinated fibers size distributions, presence of extrinsic fascicles, glomus tissue content, etc.) differentiate the vagal branches into three morphologically distinct sets: a gastric pair, a celiac pair, and a hepatic branch. The fiber counts, when considered with observations of the numbers of efferents and adventitial fibers in the nerve, suggest that the percentage of efferent fibers is much higher than in all the widely accepted estimates found in the literature: efferent fibers may represent over a quarter of the total number of fibers.

CCK enhances response to gastric distension by acting on capsaicin-insensitive vagal afferents

“…Although the vagus consists mainly of small unmyelinated C-type afferents (25), Berthoud et al (3) reported that a substantial number of intraganglionic laminar endings (IGLEs) and vagal intramuscular arrays in the stomach survive capsaicin treatment, suggesting that at least some gastric mechanoreceptive afferents are A-type afferents. Results of other experiments that used capsaicin support the hypothesis that gastric distension and CCK acted via distinct populations of vagal afferents.…”

Is-there a place for vagus nerve stimulation in inflammatory bowel diseases?

“…It is a mixed nerve composed of 80% afferent and 20% efferent fibers (Prechtl & Powley, 1990). The VN is a key element of brain-gut interactions and of the autonomic nervous system (Bonaz et al, 2017).…”

Autonomic Neuroscience: Basic and Clinical

“…In fact, this neurotoxin selectively destroys weakly myelinated A-delta or unmyelinated C afferent fibers (Jancsó et al, 1987;Hølzer, 1991;Ritter and Dinh, 1992;Blackshaw et al, 2000), fibers particularly abundant in the vagal nerve (Mei et al, 1980;Mei, 1983;Prechtl and Powley, 1990;Sengupta and Gebhart, 1994;Berthoud et al, 1997). In agreement with studies of vagotomized animals (Phillips and Powley, 1998), investigations of capsaicin-treated subjects have shown that the perivagal administration of capsaicin induces a greater food intake vs. controls at 6, 12 and 24 h after the surgical intervention, with a similar intake to that of controls at 48 and 72 h (Zafra et al, 2003).…”

“…Vagal afferents have been linked to numerous nutritive processes, especially in relation to the satiation mechanism (González and Deutsch, 1981;Smith et al, 1981;Blackshaw and Grundy, 1990;Prechtl and Powley, 1990;Davis et al, 1994;Phillips and Powley, 1998;Schwartz et al, 1999;Schwartz, 2000;Ritter, 2004). Therefore, the greater intake observed during the 24 h after capsaicin treatment can be interpreted as a consequence of the interruption of vagal neural signals involved in short-term food intake control.…”