OBJECTIVETo investigate the distribution patterns of neuron-specific enolase (NSE) and synaptophysin (SYN) during the development of human fetal stomach.

METHODSSixteen specimens of human fetal (gestational age 2 to 4 months) gastric tissues were examined with immunohistochemistry for detecting the distribution of NSE and SYN expressions in the gastric walls.

RESULTSDuring the second to fourth gestational months, NSE was strongly expressed in the nerve cells and nerve fibers of the myenteric nerve plexus of human fetal stomach. As the gestational age increased, the numbers of NSE positive cells and fibers increased gradually in the gastric submucosa, but NSE was negative in the gastric mucosa. At the second gestational month, SYN expression was negative in the mucosa but positive in the myenteric nerve plexus; during the third to fourth months, positive SYN expression was found in the mucosa, submucosa and myenteric nerve plexus of the embryonic gastric walls and its expression intensity increased with the gestational age.

CONCLUSIONSYN and NSE are both involved in the regulation of the nervous system in the gastric wall but their expressions and distributions follow different patterns during the development of human fetal stomach.

Fetus ; metabolism ; Gastric Mucosa ; metabolism ; Gestational Age ; Humans ; Immunohistochemistry ; Myenteric Plexus ; Nerve Fibers ; metabolism ; Neurons ; metabolism ; Phosphopyruvate Hydratase ; metabolism ; Stomach ; metabolism ; Synaptophysin ; metabolism

To understand the neurochemical properties of the gastric myenteric plexus of ruminants, the expression patterns of calbindin D-28k (CB), calretinin (CR), substance P (SP) and calcitonin gene-related peptide (CGRP) were explored in the Korean native goat. In gastric myenteric plexus, CB and SP immunoreactivity were observed in round- or ovalshaped neurons. CR and CGRP immunoreactivity were detected only in the nerve fibers. This immunohistochemical localization of CB, CR, CGRP and SP in the myenteric plexus of the goat stomach exhibited species-specific patterns. These findings suggest that these substances may be directly or indirectly related to the gastric functions of the goat stomach.
Animals ; Calcitonin Gene-Related Peptide ; Calcium-Binding Protein, Vitamin D-Dependent/metabolism ; Calcium-Binding Proteins/*metabolism ; Goats/*metabolism ; Immunohistochemistry/veterinary ; Myenteric Plexus/*metabolism ; Stomach/*innervation ; Substance P/metabolism

AIMTo investigate the effect of acute exhaustive exercise on gastrointestinal motility and its enteric nervous mechanisms.

METHODS24 rats were randomly divided into control group (C) and acute exhaustive exercise group (AEE). The rate of gastrointestinal transit was measured and histologic changes of nitriergic nerves in ileum myenteric plexus were observed with enzymatic histochemical and image analytic technique.

RESULTSIn the rats of AEE group, the rate of gastrointestinal transit was delayed comparing with C group (P < 0.05), the numbers of nitrergic neurons and expression levels of nitric oxide synthase (NOS) in the ileum myenteric plexus significantly increased comparing with C group (P < 0.01).

CONCLUSIONIt is possible that increase of nitrergic neurons and expression levels of NOS in the myenteric plexus of small intestine are one of the mechanisms of delay of gastrointestinal transit rate in acute exhaustive exercise rats.

Animals ; Gastrointestinal Motility ; physiology ; Gastrointestinal Transit ; physiology ; Ileum ; innervation ; Male ; Motor Activity ; Myenteric Plexus ; metabolism ; Nitrergic Neurons ; cytology ; Nitric Oxide Synthase ; metabolism ; Rats ; Rats, Sprague-Dawley

BACKGROUND/AIMS: Inflammation-induced alterations in smooth muscle contractility may be due to the effects on smooth muscle itself, neurotransmitters or enteric nerves. In dextran sulfate sodium-induced colitic rat, the delay in colonic transit was caused by decreased activity and production of neuronal nitric oxide synthase (nNOS) in the myenteric plexus of the distal colon. The aim of this study was to investigate the relationship between the delay in colonic transit and the distribution of inducible NOS (iNOS) and nNOS immunoreactive cells in the myenteric plexus of trinitrobenzene sulfonic acid (TNBS)-induced colitic guinea pig. METHODS: Sacrificed and their colonic tissues of forty-five TNBS-induced colitic guinea pigs were used to measure the colonic transit, and analyzed by immunohistochemistry. RESULTS: Colonic transit was delayed significantly at 3, 7 and 14 days after administration of TNBS. In control, nNOS immunoreactivity was present in the mucosa, submucosa, lamina propria, and ganglion cells of the myenteric plexus, while after TNBS treatment, reduced nNOS cells were found. However, the number of nNOS ganglion cells in the myenteric plexus was similar to those seen in controls. After administration of TNBS, iNOS immunoreactivity was increased in the mucosa and submucosa, but the number of iNOS positive ganglion cells in the myenteric plexus was not changed compared to control. CONCLUSIONS: It is suggested that in TNBS-induced guinea pig colitis, delayed colonic transit is not associated with the expression of nNOS nor iNOS in the myenteric plexus.
Animals ; Colitis/chemically induced/enzymology/*physiopathology ; Colon/*enzymology/innervation ; English Abstract ; *Gastrointestinal Transit ; Guinea Pigs ; Male ; Myenteric Plexus/*enzymology ; Nitric-Oxide Synthase/*metabolism ; Trinitrobenzenesulfonic Acid

Nitric oxide (NO) is a non-adrenergic, non-cholinergic neurotransmitter found in the enteric nervous system that plays a role in a variety of enteropathies, including inflammatory bowel disease. Alteration of nitrergic neurons has been reported to be dependent on the manner by which inflammation is caused. However, this observed alteration has not been reported with acetic acid-induced colitis. Therefore, the purpose of the current study was to investigate changes in nitrergic neuromuscular transmission in experimental colitis in a rat model. Distal colitis was induced by intracolonic administration of 4% acetic acid in the rat. Animals were sacrificed at 4 h and 48 h postacetic acid treatment. Myeloperoxidase activity was significantly increased in the acetic acid-treated groups. However, the response to 60 mM KCl was not significantly different in the three groups studied. The amplitude of phasic contractions was increased by Nomega-nitro-L-arginine methyl ester (L-NAME) in the normal control group, but not in the acetic acid-treated groups. Spontaneous contractions disappeared during electrical field stimulation (EFS) in normal group. However, for the colitis groups, these contractions initially disappeared, and then reappeared during EFS. Moreover, the observed disappearance was diminished by L-NAME; this suggests that these responses were NO-mediated. In addition, the number of NADPH-diaphorase positive nerve cell bodies, in the myenteric plexus, was not altered in the distal colon; whereas the area of NADPH-diaphorase positive fibers, in the circular muscle layer, was decreased in the acetic acidtreated groups. These results suggest that NO-mediated inhibitory neural input, to the circular muscle, was decreased in the acetic acid-treated groups.
Acetic Acid/toxicity ; Animals ; Colitis/chemically induced/*pathology/*physiopathology ; Colon/drug effects/enzymology/*innervation/pathology ; Indicators and Reagents/toxicity ; Male ; Muscle Contraction/drug effects ; Muscle, Smooth/drug effects/metabolism ; Myenteric Plexus/pathology ; NADPH Dehydrogenase/metabolism ; NG-Nitroarginine Methyl Ester/pharmacology ; Neuromuscular Junction/drug effects/*metabolism ; Nitrergic Neurons/drug effects/*metabolism ; Nitric Oxide/*metabolism ; Peroxidase/metabolism ; Potassium Chloride/pharmacology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the effects of motilin agonists on intracellular Ca(2+) mobilization in primary cultured rat myenteric neurons.

METHODSMotilin-induced and erythromycin-induced intracellular Ca(2+) signaling was studied in primary cultures of rat myenteric neurons using the radiometric Ca(2+) indicator Furo3/AM with a laser confocal microscope.

RESULTSIn Hank's solution, 10(-8), 10(-7), and 10(-6) mol/L motilin could elevate intracellular Ca(2+) concentration ([Ca(2+)]i) to the peak levels of 10.6-/+2.1, 15.9-/+1.2, and 30.6-/+3.7 respectively with their relative percentage change in fluorescent intensity of (40.1-/+6.3)%, (63.0-/+11.2)%, and (100.8-/+18.4)% respectively, indicating the dose-dependent effect of motilin on [Ca(2+)]i. In Hank's solution, 10 microg/ml erythromycin could induce the elevation of [Ca(2+)]i to the average peak of 23.2-/+5.6 with the relative percentage change in fluorescent intensity of (82.8-/+13.0)%. When pretreated with the antibody against motilin receptor in Hank's solution, the effect of 10 microg/ml erythromycin was almost inhibited completely.

CONCLUSIONMotilin can increase [Ca(2+)]i, and erythromycin also has this effect by binding to motilin receptor.

Animals ; Animals, Newborn ; Calcium ; metabolism ; Calcium Signaling ; drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Erythromycin ; pharmacology ; Microscopy, Confocal ; Motilin ; pharmacology ; Myenteric Plexus ; cytology ; metabolism ; Neurons ; cytology ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Gastrointestinal Hormone ; agonists ; Receptors, Neuropeptide ; agonists