Topography of efferent vagal innervation of the rat gastrointestinal tract

1991 ◽  
Vol 260 (1) ◽  
pp. R200-R207 ◽  
Author(s):  
H. R. Berthoud ◽  
N. R. Carlson ◽  
T. L. Powley

The gastrointestinal territories innervated by the gastric, celiac, and hepatic abdominal vagi were identified in rats with selective branch vagotomies by means of 1) anterograde tracing with the carbocyanine dye DiI injected into the dorsal motor nucleus and 2) measurement of cervical vagal stimulation-induced motility responses throughout the gut axis. Presence of DiI-labeled vagal terminals in the myenteric plexus and evoked motility responses were well correlated across the sampled gastrointestinal (GI) sites. In animals with only the two gastric branches intact, the entire stomach and the most proximal duodenum showed significant motility responses and were densely innervated, having DiI-labeled vagal terminals in almost every ganglion. The hepatic branch was found to primarily innervate the duodenum, with minor projections to the distal antral stomach and the intestines. The two celiac branches were found to almost exclusively innervate the jejunum, ileum, cecum and entire colon, and, together with the other vagal branches, the duodenum. Therefore, while there is some degree of specific innervation by the abdominal vagal branches of the oral-to-anal gut axis, which could be called "viscerotopic," the considerably overlapping innervation of the duodenum does not satisfy a viscerotopy criterion and needs further functional analysis.

1990 ◽  
Vol 258 (2) ◽  
pp. R523-R530 ◽  
Author(s):  
H. R. Berthoud ◽  
T. L. Powley

To define the vagal circuitry mediating the cephalic phase insulin response (CPIR), this reflex was measured in conscious, freely moving rats that had previously undergone selective abdominal vagotomies that spared different columnar subpopulations of dorsal motor nucleus of the vagus (dmnX) neurons. The CPIR was defined as an increase of plasma insulin from basal at 2 min after the start of ingestion. The CPIR measured in peripheral blood after chow ingestion was reliable and significant (P less than 0.05) in rats with all branches intact, +24.9 +/- 5.1 microU/ml (+130% increase from basal); rats with only the two gastric branches and the hepatic branch intact, +27.0 +/- 3.5 microU/ml (+153%); and rats with only the hepatic branch intact, +13.5 +/- 4.8 microU/ml (+188%). No significant response occurred in animals with only the two celiac branches intact, +1.8 +/- 1.8 microU/ml (+15%) or in those with none of the branches intact, +3.9 +/- 3.3 microU/ml (+21%). The CPIRs measured in portal vein blood were generally larger but showed the same pattern across groups. Plasma glucose measurements of portal vein blood indicated that with chow ingestion no significant absorption had occurred by 2 min, whereas with either milk or glucose intake absorption did occur. Subsequent bilateral electrical cervical vagal stimulation-induced insulin and glucagon responses in the same animals under anesthesia showed the same branch dependency. It is concluded that the CPIR is mediated by the two gastric and the hepatic branches but not the two celiac vagal branches. The perikarya of the preganglionics innervating the pancreatic B-cells are contained within a large pool occupying the two medial columns of the dmnX.


1987 ◽  
Vol 253 (2) ◽  
pp. R361-R370 ◽  
Author(s):  
T. L. Powley ◽  
E. A. Fox ◽  
H. R. Berthoud

A new protocol that provides a sensitive, reliable, and practical test for completeness of selective as well as total subdiaphragmatic vagotomies is described. This protocol employs a microscopic inventory of retrogradely labeled neurons in topographically distinct regions of the dorsal motor nucleus to determine which vagal branches have been surgically destroyed. Physiological experiments for validation and observations on the use of the method with 243 rats indicate that the protocol described can assess total as well as at least 11 different types of selective subdiaphragmatic vagotomies, including surgeries for which no assays have existed. Furthermore, the technique can identify cases where a branch is only partially destroyed. Other strengths include the facts that the protocol provides a simultaneous inventory of the different branches in a single test, is not influenced by the general health of the animal, and does not interfere with concurrent behavioral or physiological tests. Limitations include the facts that the tracer inventory requires a minimal survival period, can only be done postmortem, and has low resolution for cuts of the vagal hepatic branch. Aspects of the protocol critical to its implementation, including specifics for using the fluorescent tracer true blue, are discussed. Other tracers with similar diffusion characteristics, such as fluoro-gold and fast blue, can be used with equal effectiveness with this protocol.


2002 ◽  
Vol 88 (1) ◽  
pp. 49-63 ◽  
Author(s):  
Xueguo Zhang ◽  
Ronald Fogel

Data have shown that the paraventricular nucleus of the hypothalamus (PVN) and the dorsal motor nucleus of the vagus (DMNV) play important roles in the regulation of gastrointestinal function and eating behavior. Anatomical studies have demonstrated direct projections from the PVN to the DMNV and physiological studies showed that the DMNV mediates many of the effects of PVN stimulation and electrical current stimulation of the PVN excites a subset of DMNV neurons. The aim of this study was to characterize the role of glutamate receptors in the excitatory influence of the PVN on gut-related DMNV neurons. Using single-cell recording techniques, we determined the effects of kynurenic acid, 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX), anddl-2-amino-5-phosphonopentanoic acid (dl-AP5) on the increase in firing rate due to electrical current stimulation of the PVN. In initial experiments, we studied 24 DMNV neurons excited by electrical current stimulation of the PVN. Kynurenic acid, a broad-spectrum glutamate receptor antagonist, prevented the PVN effect in 22 neurons and significantly attenuated the effect in the other cells. Nine of these neurons demonstrated an inhibition in firing rate with PVN stimulation after pretreatment with kynurenic acid. In a separate group of 12 neurons, we determined the effects of CNQX (1.2 nmol) injected into the DMNV. This AMPA receptor antagonist completely blocked the excitatory response to PVN stimulation of six DMNV neurons and significantly attenuated the response of the other six DMNV neurons. The addition of 1.2 nmol dl-AP5, a N-methyl-d-aspartate (NMDA) receptor antagonist, further attenuated the response to PVN stimulation in four of the five DMNV neurons that were still excited after CNQX treatment. The fifth neuron demonstrated PVN- induced inhibition of firing rate after treatment with CNQX and dl-AP5. In a separate group of 11 DMNV neurons excited by electrical stimulation of the PVN,dl-AP5 partially attenuated the excitatory responses of only four DMNV neurons and did not block the excitation of any cells. The mean latency (14 neurons tested) from the PVN to the DMNV was 37.71 ± 2.40 (SE) ms. Monosynaptic action potentials and excitatory postsynaptic potentials were demonstrated in three DMNV neurons by intracellular recording. Our results indicate that glutamate released from PVN neurons projecting to the DMNV excite the gut-related vagal motor neurons by acting predominantly on the AMPA receptor. The NMDA receptor plays only a minor role in the excitatory effect.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
L. A. Ballsmider ◽  
A. C. Vaughn ◽  
M. David ◽  
A. Hajnal ◽  
P. M. Di Lorenzo ◽  
...  

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.


1985 ◽  
Vol 248 (1) ◽  
pp. H89-H97 ◽  
Author(s):  
N. Takahashi ◽  
M. J. Barber ◽  
D. P. Zipes

The route efferent vagal fibers travel to reach the left ventricle is not clear and was the subject of this investigation. We measured left ventricular and septal effective refractory period (ERP) changes during vagal stimulation and a constant infusion of norepinephrine, before and after phenol was applied at selected sites of the heart to interrupt efferent vagal fibers that may be traveling in that area. Phenol applied to the atrioventricular (AV) groove between the origin of the right coronary artery anteriorly to the posterior descending branch of the circumflex coronary artery completely eliminated vagal-induced prolongation of ERP in the anterior and posterior left ventricular free wall and reduced, but did not eliminate, ERP prolongation in the septum. A large (3-cm radius) epicardial circle of phenol prevented vagal-induced ERP prolongation within the circle in all dogs, while a small (1-cm radius) epicardial circle of phenol failed to prevent vagal-induced ERP changes within the circle in any dog. An intermediate (2-cm radius) circle eliminated vagal effects on ERP in 13 of 18 dogs. Arcs of phenol, to duplicate the upper portion of the circle, applied sequentially from apex to base eliminated efferent vagal effects only when painted near or at the AV groove. We conclude that the majority of efferent vagal fibers enroute to innervate the anterior and posterior left ventricular epicardium cross the AV groove within 0.25-0.5 mm (depth of phenol destruction) of the epicardial surface.(ABSTRACT TRUNCATED AT 250 WORDS)


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Xinyan Gao ◽  
Yongfa Qiao ◽  
Baohui Jia ◽  
Xianghong Jing ◽  
Bin Cheng ◽  
...  

Previous studies have demonstrated the efficacy of electroacupuncture at ST36 for patients with gastrointestinal motility disorders. While several lines of evidence suggest that the effect may involve vagal reflex, the precise molecular mechanism underlying this process still remains unclear. Here we report that the intragastric pressure increase induced by low frequency electric stimulation at ST36 was blocked by AP-5, an antagonist of N-methyl-D-aspartate receptors (NMDARs). Indeed, stimulating ST36 enhanced NMDAR-mediated, but not 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl)propanoic-acid-(AMPA-) receptor-(AMPAR-) mediated synaptic transmission in gastric-projecting neurons of the dorsal motor nucleus of the vagus (DMV). We also identified that suppression of presynapticμ-opioid receptors may contribute to upregulation of NMDAR-mediated synaptic transmission induced by electroacupuncture at ST36. Furthermore, we determined that the glutamate-receptor-2a-(NR2A-) containing NMDARs are essential for NMDAR-mediated enhancement of gastric motility caused by stimulating ST36. Taken together, our results reveal an important role of NMDA receptors in mediating enhancement of gastric motility induced by stimulating ST36.


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