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PubMed1986

Somatostatin immunoreactive nerve elements in the rat small intestine: light and electron microscopic studies.

Somatostatin-containing nerve elements were identified by light and electron microscopic immunocytochemistry in the rat small intestine. Labelled nerve cell bodies were found in the submucous plexus. In the myenteric plexus and the mucosa, numerous somatostatin positive fibers were found. Labelled fibers were observed in the vicinity of blood vessels, close to the smooth muscle cell membrane and to the lamina basalis of epithelial cells. In both plexuses, there were many synapses between the labelled and unlabelled nerve elements. After transection of the nn. mesenteric some of the degenerated nerve fibers originating outside the wall of the small intestine contained also somatostatin immunoreactivity. These observations suggest that somatostatin nerves not only influence the blood flow, but participate in regulation of smooth muscle activity and, by the aid of their interneuronal synapses they have a regulatory or transmitter effect on the other intrinsic nerve elements.

Animals↗

PubMed1997

The polarity of neurochemically defined myenteric neurons in the human colon.

BACKGROUND & AIMS: Functional classes of enteric neurons in small mammals can be determined by neurochemical coding and axonal projections. The aim of this study was to describe the projections of vasoactive intestinal peptide (VIP)-, tachykinin (TK)-, and calretinin-immunoreactive (IR) interneurons and circular muscle motor neurons in human colon. METHODS: Human colonic myenteric neurons were retrogradely filled with 1,1'-didodecyl 3,3,3',3'-indocarbocyanine perchlorate (DII) from either the myenteric plexus or the circular muscle layers in organotypic culture preparations. The preparations were then labeled with antisera, and the position and immunoreactivity of DII-filled neurons was recorded. RESULTS: Nine percent of circular muscle motor neurons were labeled with TK immunoreactivity and these projected orally; 22% were VIP-IR and projected anally. Fifty-one percent of myenteric neurons that projected anally to the myenteric ganglia were VIP-IR and none were TK-IR. In contrast, 23% of neurons projecting orally were TK-IR but only 2% were VIP-IR. Calretinin immunoreactivity was present in 23% of neurons projecting anally and 3% projecting orally within the myenteric plexus. Six percent of circular muscle motor neurons had Dogiel type II morphology, and 50% of these were TK-IR. CONCLUSIONS: Circular muscle motor neurons and myenteric interneurons with TK, VIP, and calretinin immunoreactivity in the human colon have distinct projections and polarity.

Adult↗

PubMed2003

[Functional difference of prokinetics depending on subtypes and localization of receptor in alimentary tract].

Interaction of function and localization of receptors, especially the 5-hydroxytryptamine4 (5-HT4) receptor was examined in relation to the motility of gastrointestinal tract. The responses mediated by stimulation of 5-HT4 receptor appear to differ with different localization of receptor. The 5-HT4 receptor-mediated acceleration of acetylcholine (ACh) release in the preparations isolated from gastric antrum and corpus, but not fundus, of guinea pig corresponded to the presence of 5-HT4 receptor in the myenteric plexus. The 5-HT4 receptor-mediated response was predominant in the 5-HT-induced acceleration of motility associated with ACh release in the intestine of the whole body of dogs, and the 5-HT4 receptor was localized on the myenteric plexus of dog intestine. Local administration of GABA into intestinal marginal artery reduced the motility associated with ACh release in the intestine of whole body of dogs, and thus response via the inhibitory GABAB receptor was more predominant than that via excitatory GABAA receptor. The GABAB receptor is the first G protein-coupled receptor discovered to form heterodimers, consisted of GABAB1 and GABAB2. There are isoforms of GABAB1, from GABAB1(a) to GABAB1(g), and therefore the function and localization of the GABAB receptor may vary with the different isoforms of GABAB1.

Animals↗

PubMed2001

Selective knockout of intramuscular interstitial cells reveals their role in the generation of slow waves in mouse stomach.

1. Intracellular recording techniques were used to compare the patterns of electrical activity generated in the antral region of the stomachs of wild-type and W/W(V) mutant mice. Immunohistochemical techniques were used to determine the distribution of c-kit-positive interstitial cells of Cajal (ICC) within the same region of the stomach. 2. In wild-type mice interstitial cells were found at the level of the myenteric plexus (ICC(MY)) and distributed within the smooth muscle bundles (ICC(IM)). In these preparations slow waves, which consisted of initial and secondary components, were detected. 3. In W/WV mutant mice ICC(MY) could be identified at the level of the myenteric plexus but ICC(IM) were not detected within smooth muscle bundles. Intracellular recordings revealed that smooth muscle cells generated waves of depolarization; these lacked a secondary component. 4. These results indicate that the secondary regenerative component of a slow wave is generated by ICC(IM). Thus the depolarization arising from the pacemaker cells, ICC(MY), is augmented by ICC(IM), so causing a substantial membrane depolarization in the circular muscle layer. Rather than contributing directly to rhythmical electrical activity, smooth muscle cells appear to depolarize at the command of the two subpopulations of ICC.

Animals↗

PubMed2002

The longitudinal smooth muscle layer of the pig small intestine is innervated by both myenteric and submucous neurons.

Originally, intestinal motility was thought to be exclusively regulated by myenteric neurons. Some years ago, however, it was demonstrated in large mammals that submucous neurons also participate in the innervation of the circular smooth muscle layer. To date, no information is available about the submucous innervation of the longitudinal smooth muscle layer (LM). This study provides evidence that in the small intestine of large mammals, the LM is innervated not only by the myenteric plexus, but also by the inner and outer submucous plexuses (ISP and OSP). In the porcine small intestine, the involved neurons can be subdivided into the following neurochemically distinct populations: leu-enkephalin (ENK)- and/or substance P (SP)-IR neurons and nitric oxide synthase (NOS)- and/or vasoactive intestinal polypeptide (VIP)-IR neurons. In the myenteric plexus, the majority of VIP- and/or NOS-IR neurons and ENK(+)/SP(-)-IR neurons exhibit descending projections, whereas ENK(+)/SP(+)-IR neurons preferentially have ascending projections. The ENK(-)/SP(+)-IR neurons do not show a polarized pattern. In the OSP, only ENK(+)/SP(-)- and VIP(+)/NOS(-)-IR neurons display a polarized (descending) projection pattern, whereas no polarization can be noted in the ISP. Morphological analysis of the traced neurons revealed that, in general, myenteric descending LM motor neurons have larger cell bodies than ascending ones and, in addition, myenteric descending VIP- and/or NOS-IR neurons have longer projections than ENK and/or SP-IR neurons. In conclusion, the present study demonstrates the involvement of not only myenteric, but also submucous neurons in the innervation of the LM. The two major populations are descending nitrergic neurons and ascending tachykinergic motor neurons, but also other subpopulations with specific projection patterns and neurochemical features have been identified.

Animals↗

PubMed1999

Morphologic and quantitative study of the myenteric neurons of the jejunum of malnourished rats (Rattus norvegicus).

We studied the effects of maternal proteic desnutrition on the neurons of the myenteric plexus of the jejunum of rats from Rattus norvegicus species. It was used litters of female rats which received diet with normal proteic level during gestation and lactation (group NN), normal diet during gestation and hypoproteic diet during lactation (group ND); hypoproteic diet during gestation and normal diet during lactation (group DN); hypoproteic diet during both gestation and lactation (group DD). After weaning all the animals received diet of normal proteic level until the 60th day of age, when they were killed. The jejunum of the animals was subjected to whole-mount preparations stained by the method of Giemsa and used for the morphologic and quantitative analyses of the neurons of the myenteric plexus. We verified that maternal proteic malnutrition does not cause decrease on the number of myenteric neurons per unit area of jejunum in rats, but elicits mechanisms which assure that, when the animal again receives normal proteic level diet (22%) there occurs storage of proteic material on the cytoplasm of the neurons, thus rendering them larger and strongly basophylic.

Animals↗

PubMed1990

Effect of diabetes in the BB Wistar rat on the peptidergic component of the enteric innervation.

Whole mount preparations of the small intestine from Wistar, normoglycemic 90-day diabetic BB, hyperglycemic 90-day diabetic BB and age-matched nondiabetic BB rats were immunostained to determine the extent of the peptidergic innervation. The neuropeptides examined were vasoactive intestinal peptide, neuropeptide Y, substance P. calcitonin gene-related peptide, galanin and somatostatin. The extent of the peptidergic innervation in the submucous and myenteric plexuses from the control Wistar, nondiabetic BB and normoglycemic diabetic BB rats was identical. In the submucous plexus of the hyperglycemic diabetic BB rats there was a marked reduction in the number of somatostatin-immunoreactive neurons and nerve fibres. Substance P and calcitonin gene-related peptide which are colocalized in a proportion of the somatostatin neurons were unaffected. In the myenteric plexus of the hyperglycemic diabetic BB rats the number and intensity of staining of the galanin-immunoreactive nerve fibers was markedly increased. Galanin has not been observed to colocalize with any of the other neuropeptides examined.

Animals↗

PubMed2003

Morphology and distribution of nitric oxide synthase-, neurokinin-1 receptor-, calretinin-, calbindin-, and neurofilament-M-immunoreactive neurons in the myenteric and submucosal plexuses of the rat small intestine.

Characterization of the enteric neurons is vital for understanding their physiological role. We have used single and dual label fluorescence and peroxidase-based immunohistochemistry in myenteric and submucosal whole mounts from the rat small intestine to evaluate the morphology and distribution of enteric neurons immunoreactive for the following phenotypic antigens: neuronal nitric oxide synthase (NOS), neurokinin-1 receptor (NK-1R), calretinin (Calr), calbindin (Cal), and neurofilament-M (NF-M). NOS-immunoreactive neurons had Dogiel type I morphology, were abundant in the myenteric plexus compared to the submucosal plexus, and never coexpressed NK-1R immunoreactivity. NK-1R- and Calr-immunoreactive neurons had Dogiel type II morphology and were distributed comparably in both plexuses. NK-1R and Calr-immunoreactivity were coexpressed in many of the same neurons. Calbindin-immunoreactive neurons exhibited four distinct morphologies: small and large Dogiel type II neurons, Dogiel type I neurons, and small elongated neurons. These neurons were significantly fewer in number in the myenteric plexus compared to the submucosal plexus. Neurofilament-M-immunoreactive neurons had three morphologies, Dogiel type II neurons, small Dogiel type II neurons, and a less common subpopulation of small, elongated, multipolar neurons. These neurons were also fewer in number in the myenteric plexus compared to the submucosal plexus. The distribution of these phenotypic markers may assist future work that elucidates the functional activities of these enteric neurons such as control of intestinal motility and adaptation to the entry of gastric contents.

Animals↗

PubMed1992

Nitric oxide synthase activity in infantile hypertrophic pyloric stenosis.

BACKGROUND: Hypertrophic pyloric stenosis is a common infantile disorder characterized by enlarged pyloric musculature and gastric-outlet obstruction. Its physiopathologic mechanism is not known, but a defect in pyloric relaxation (pylorospasm) has been postulated. Nitric oxide is a mediator of relaxation in the mammalian digestive tract, raising the possibility that pylorospasm could be caused by a defect in nitric oxide production. Since neuronal nitric oxide synthase and NADPH diaphorase are identical, we used the NADPH diaphorase histochemical reaction to study the distribution of nitric oxide synthase in pyloric tissue from patients with infantile hypertrophic pyloric stenosis. METHODS: We studied pyloric tissue from nine infants with infantile hypertrophic pyloric stenosis and seven control infants and children. Cryostat sections were processed for NADPH diaphorase histochemical analysis. A polyclonal tau antiserum was used to identify the enteric nervous system by immunohistochemical methods. RESULTS: NADPH diaphorase activity was restricted to the enteric nervous system and blood vessels. In the pyloric tissues from the control patients, intense diaphorase activity was present in the nerve fibers of the circular musculature, in the neurons and nerve bundles of the myenteric plexus, and in some nerve fibers of the longitudinal musculature. In the pyloric tissues from patients with infantile hypertrophic pyloric stenosis, the enteric nerve fibers in the hypertrophied circular musculature were enlarged and distorted and did not contain diaphorase activity, whereas the activity in the myenteric plexus and the longitudinal musculature was preserved. CONCLUSIONS: We suggest that a lack of nitric oxide synthase in pyloric tissue is responsible for pylorospasm in infantile hypertrophic pyloric stenosis.

Amino Acid Oxidoreductases↗

PubMed1998

NADPH-diaphorase positive myenteric neurons in the ileum of guinea-pig, rat, rabbit and cat: a comparative study.

The nitrergic system of the ileal myenteric plexus of four mammalian species was studied by means of NADPH diaphorase histochemistry which in aldehyde-fixed tissue stains only those cells that contain the constitutive, calcium-dependent nitrogen monoxide synthase isoenzyme. Since previous studies assumed minor species-specific anatomical variations, we sought similarities and differences in the nitrergic innervation pattern of the ileal musculature. In rat and guinea-pig, the ratio of nitrergic cells slightly exceeds 20%, in rabbit it is close to this number (16%), and it is lowest in cat (about 10%). The nitrergic neurons target the circular muscle layer in all investigated species where they participate in inhibitory motoric transmission. Apart from this, some elements of the sensory innervation of the circular musculature may derive from nitrergic neurons in rat and rabbit. The tertiary plexus (longitudinal muscles) is strongly supplied by NADPH diaphorase positive fibres in rat, moderately in guinea-pig and cat and not at all in rabbit. The rest of the nitrergic neurons may serve as inhibitory interneurons and control other (probably excitatory motor) neurons in the myenteric plexus. We conclude that the diverse physiological and pharmacological properties of the nitrergic system described in the small intestine in different species can be connected with the anatomical heterogeneity of its elements.

Animals↗

PubMed1997

Stimulation by enkephalins of D-glucose absorption in rabbit ileum.

In intact tissue, DAGO ([D-Ala2, MePhe4, Gly-ol5]enkephalin; 10(-5) M; mu-ligand; addition on the serosal side) stimulated D-glucose absorption and D-glucose-dependent variations in short-circuit current (delta Isc,glu); naloxone (10(-6) M) antagonized these effects. DADLE ([D-Ala2, D-Leu5]enkephalin, mainly a delta-ligand; 10(-5) M) and (pCl-Phe4)-DPDPE ([D-pen2, p-chloro-Phe4, D-Pen5]enkephalin, a more selective delta-ligand; 10(-5) M) did not significantly stimulate delta Isc,glu (addition on the serosal side). In the absence of the muscularis and myenteric plexus or using intact tissue treated with tetrodotoxin (TTX; 3 x 10(-7) M), DAGO was unable to increase delta Isc,glu. Addition of DAGO to the mucosal side did not induce any variations in delta Isc,glu. In conclusion, DAGO is able to increase D-glucose absorption by interacting with mu-receptors located in the myenteric plexus.

Animals↗

PubMed1998

Human defunctionalized colon: a histopathological and pharmacological study of muscularis propria in resection specimens.

Despite the regression of "diversion colitis," temporary functional disorders after bowel continuity restoration could be caused by changes in the smooth muscle of excluded segments; however, studies on the muscularis propria have yielded contradictory results. This study was aimed at evaluating possible histopathological changes in muscular layers and motility of the defunctionalized human colon. Ten patients with defunctionalized colorectum (group A) and 10 controls (group B) underwent restorative or primary resection surgery. Strips were taken proximal to the colostomy (specimens A1) and the defunctionalized segment (specimens A2), and from the proximal (specimens B1) and distal extremity (specimens B2) of resected colons. Measurements of the thickness of the muscularis propria and of the volume density of the myenteric plexus, as well as of spontaneous motility and responses to electrical and pharmacological stimulation were taken. The muscularis propria was thicker in A2 than in A1 specimens (P = 0.004) and in B2 than in B1 specimens (P = 0.007). No differences were recorded either in the myenteric plexus volume density or in colonic motility. No differences were recorded in intergroup comparisons. As no structural or functional changes related to defunctionalization were found, clinical disorders after colorectal restoration could rather result from underlying colonic pathology and/or incomplete distal colon resection.

Case-Control Studies↗

PubMed2002

Clinical and morphofunctional features of idiopathic myenteric ganglionitis underlying severe intestinal motor dysfunction: a study of three cases.

Ganglionitis, i.e., the inflammatory neuropathy characterized by a marked lymphoplasmacellular infiltrate in the myenteric plexus, may underlie a variety of paraneoplastic, infectious, or neurological disorders, although occasional cases are idiopathic in origin. We report clinical, manometric, morphofunctional, and immunological features of three cases of idiopathic ganglionitis. All patients had megacolon and underwent surgery for repeated episodes of intestinal subocclusion. Esophageal, GI, and colonic manometry performed in one patient showed dysmotility of the whole gut. Histological examination of colonic and ileum specimens identified a prominent lymphoplasmacellular infiltrate within the myenteric plexus along with a marked decrease of a wide array of neuronal peptides/transmitters. In one patient, tissue analysis revealed progressive neuronal changes up to marked myenteric neuron damage. The inflammatory infiltrate in all patients comprised CD4+ and CD8+ T lymphocytes. Abundance of both subclasses of lymphocytes suggests that immune-mediated mechanisms were responsible for neuronal degeneration. In one patient, systemic steroid therapy brought a significant clinical improvement. The immunosuppressive approach deserves further investigation in patients with severe gut motor abnormalities attributable to idiopathic myenteric ganglionitis.

Adult↗

PubMed1996

Acrylamide-induced neuropathic changes in rat enteric nerves: similarities with effects of streptozotocin-diabetes.

The effect of acrylamide intoxication (a widely used model for autonomic neuropathy) on the fluorescence intensity and density of catecholamine- and peptide-containing nerve fibres and tissue content of noradrenaline and the peptides vasoactive intestinal polypeptide, calcitonin gene-related peptide, substance P and neuropeptide Y in the enteric nerves of rat ileum was examined. Histochemical and immunohistochemical techniques were used to localize catecholamine- and peptide-containing nerve fibres. The tissue content of noradrenaline was measured using high-performance liquid chromatography, and an enzyme-linked immunosorbent assay technique was used to determine the tissue content of the peptides investigated. Acrylamide intoxication caused a significant decrease in the density of catecholamine-containing nerve fibres and tissue content of noradrenaline in the myenteric plexus of rat ileum. A decrease in tissue content and immunoreactivity of calcitonin gene-related peptide and an increase in vasoactive intestinal polypeptide was seen in the myenteric plexus of ileum from acrylamide-intoxicated rats. In the submucous plexus, the acrylamide treatment caused a decrease in calcitonin gene-related peptide immunoreactivity and an increase in vasoactive intestinal polypeptide and neuropeptide Y immunoreactivity. There was no change in either tissue content or immunoreactivity of substance P in both myenteric and submucous plexuses of the treated rat ileum. These changes have a striking similarity with those found in the enteric nerves of streptozotocin-diabetic rat ileum, suggesting the possible presence of an underlying common mechanism(s) in the development of neuropathic changes in the autonomic nerves of acrylamide-intoxicated and streptozotocin-diabetic rats.

Acrylamide↗

PubMed1997

Limited excitatory local effector function of gastric vagal afferent intraganglionic terminals in rats.

Intraganglionic laminar endings (IGLEs) are complex terminal structures of vagal afferent origin, distributed throughout the myenteric plexus of the esophagus and gastrointestinal tract and without a known function. They may serve local effector function by means of peripheral axon reflexes, analogously to dorsal root afferents. To test this possibility, vagal afferent fibers were antidromically activated by suprathreshold electrical stimulation of the cervical vagus nerve in anesthetized rats that underwent prior supranodose vagotomy, and responses of myenteric neurons were monitored with Fos immunocytochemistry. Stimulation of vagal afferents produced Fos expression in a slightly, but significantly, higher proportion of myenteric plexus neurons of the gastric corpus (1.02 +/- 0.21%, P < 0.05) and esophagus (1.59 +/- 0.46%, P < 0.05) than in control animals with sham-stimulation (corpus, 0.12 +/- 0.05%; esophagus, 0.18 +/- 0.18%). Stimulation of vagal efferents produced widespread Fos induction in myenteric neurons. Given the many enteric neurons in close anatomic contact with IGLEs and the low proportion of Fos activated neurons after selective afferent stimulation, the results do not support a widespread excitatory local effector function of IGLEs. However, inhibitory effects and/or weak excitatory synaptic inputs that do not engage Fos expression cannot be ruled out.

Analysis of Variance↗

PubMedDate not supplied

Opioid dependence in myenteric neurons innervating the circular muscle of guinea-pig ileum.

Guinea-pigs were treated with morphine for 6-8 days by subcutaneous implantation of pellets, each containing a mixture of morphine base (120 mg) and morphine hydrochloride (35 mg). Each guinea-pig received a single pellet. Mechanical activity of the circular muscle was recorded in vitro in preparations comprising the circular muscle and myenteric plexus. Exposure to morphine was maintained by addition of 1 microM morphine to the organ baths. After 90 min, morphine was withdrawn, either by repeatedly washing tissues in morphine-free Krebs' solution, or by addition of naloxone to reduce the occupancy of the opioid receptors by morphine. Withdrawal of morphine resulted in markedly enhanced contractile activity compared with that in circular muscle-myenteric plexus preparations from untreated control guinea-pigs. The withdrawal contractions were abolished by tetrodotoxin (600 nM) and greatly reduced by hyoscine (1 microM), indicating that they resulted from action potential discharge in myenteric neurons that release acetylcholine onto the circular muscle. Activation of the cholinergic excitatory motor neurons was not secondary to synaptic activation by cholinergic interneurons, because hexamethonium (100 microM) did not affect withdrawal contractions. The withdrawal response may therefore arise in the cholinergic excitatory motor neurons themselves, or in neurons that activate them via noncholinergic mechanisms.

Animals↗

PubMed1983

Surfactants selectively ablate enteric neurons of the rat jejunum.

Surfactants, a group of nonspecific membrane perturbating substances, can cause nerve damage. Various concentrations of the cationic surfactants benzalkonium chloride (BAC) and benzethonium chloride, the anionic surfactants sodium ricinoleate, dioctyl sodium sulfosuccinate and sodium lauryl sulfate and the nonionic surfactant Triton X-100 were applied to the serosal surface of the rat jejunum every 5 min for 0.5 hr and then rinsed off with saline. Thirty days after surfactant application, the treated and an untreated segment of jejunum were removed and examined histologically. All surfactants which were tested significantly reduced the number of ganglion cells in the myenteric plexus. In addition, sodium ricinoleate significantly reduced the number of ganglion cells in the submucosal plexus. Higher concentrations of the cationic agents BAC and benzethonium chloride caused a generalized tissue damage including disruption of the smooth muscle, lymphocytic infiltration, intestinal perforation and death. Using BAC as a prototype surfactant, peptidergic neuron distribution and gut electrical activity were examined. BAC treatment markedly reduced the immunoreactivity of somatostatin, substance P, met-enkephalin and vasoactive intestinal peptide in the myenteric plexus. In addition, the electric properties of the smooth muscle were altered. BAC treatment resulted in an erratic, markedly distorted basic electric rhythm and an alteration in spike potential generation. These studies demonstrate that surfactants in appropriate concentrations selectively ablate the myenteric neurons and alter peptidergic neuron distribution and gut electrical parameters in the rat jejunum.

Animals↗

PubMed1997

Vagal preganglionic projections to the enteric nervous system characterized with Phaseolus vulgaris-leucoagglutinin.

The patterns and extent of vagal preganglionic divergence and convergence within the gastrointestinal tract of the rat were characterized with the anterograde tracer Phaseolus vulgaris-leucoagglutinin (PHA-L). Three weeks after tracer was iontophoretically injected into two to four sites within the dorsal motor nucleus of the vagus, wholemounts of perfused gut organs (stomach, duodenum, cecum) were prepared, counterstained with Cuprolinic blue, and processed for PHA-L using the avidin biotin complex with diaminobenzidine. Controls included animals injected with PHA-L after intracranial deafferentations. Well-positioned injections labeled an extremely dense and intricate network of varicose efferent axons throughout the gastric myenteric plexus (including that of the fundus). Individual fibers collateralized extensively, forming a variety of pericellular arborizations and terminal complexes made up of both en passant and end swellings. Single axons frequently innervated subsets of neurons within ganglia. Most enteric neurons were contacted by varicosities of more than one vagal fiber. The patterns of vagal preganglionic fibers in the duodenal and cecal myenteric plexuses resembled the organization in the stomach in many aspects, but the projections in each organ had distinctive characteristics, and label was less dense in the intestines than in the stomach. Vagal preganglionic fibers directly innervated submucosal ganglia, although sparsely. Brainstem injections of PHA-L retrogradely labeled a few myenteric neurons in the corpus, fundus, and duodenum: These "gastrobulbar" and "duodenobulbar" neurons received reciprocal vagal preganglionic innervation. Finally, the PHA-L that spread to the nucleus of the solitary tract occasionally produced transganglionic labeling of afferent intramuscular arrays (gastric fundus). The results of this paper provide strong evidence that the traditional "command neuron" or "mother cell" hypotheses of vagal-enteric organization should be abandoned for an integrative neural network model.

Animals↗