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PubMed1995

Benzimidazolones and renzapride facilitate acetylcholine release from guinea-pig myenteric plexus via 5-HT4 receptors.

The effects of the 5-HT4 receptor agonists BIMU 8, BIMU 1, renzapride and of the 5-HT1p receptor agonist 5-hydroxyindalpine on basal and electrically evoked outflow of tritium were studied in guinea-pig longitudinal muscle myenteric plexus preparations preincubated with [3H]choline. Muscle contractions were recorded simultaneously. BIMU 8 caused a calcium dependent and tetrodotoxin sensitive increase in basal [3H]outflow that was assumed to represent release of [3H]acetylcholine. In addition, BIMU 8 enhanced the release of [3H]acetylcholine and twitch contractions evoked by submaximal electrical stimulation. Ondansetron (1 mumol/l) did not change the effects of BIMU 8, but DAU 6285 and tropisetron (each 1 mumol/l) competitively antagonized the various facilitatory effects of BIMU 8 with pA2 values of 7.0-7.2 (DAU 6285) and 7.0-7.3 (tropisetron). The phosphodiesterase inhibitors IBMX and rolipram did not increase the effects of BIMU 8. BIMU 1 and renzapride also concentration-dependently increased basal release of acetylcholine, and release and contractions caused by submaximal stimulation. The effects of BIMU 1 and renzapride were competitively antagonized by 1 mumol/l tropisetron (pA2 6.6-7.1). The EC50 values for the increase in the evoked [3H]acetylcholine release and contractions were closely similar. 5-Hydroxyindalpine did not change basal release and slightly inhibited the evoked release of [3H]acetylcholine. Release of acetylcholine and contractions elicited by submaximal stimulation were strongly inhibited by (+)-tubocurarine which indicates that nicotine ganglionic transmission is involved in this kind of release. The results suggest that BIMU 8, BIMU 1 and renzapride stimulate 5-HT4 receptors at cholinergic interneurones and thereby facilitate nicotinic ganglionic transmission in the myenteric plexus.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed2005

Pharmacological characterisation of voltage-dependent Ca2+ channels in isolated ganglia from the myenteric plexus.

Voltage-dependent Ca2+ channels of fura-2-loaded ganglionic cells from the myenteric plexus of newborn rats were pharmacologically characterised. In contrast to completely dissociated myenteric cells, intact ganglia showed a stronger loading with the Ca2+-sensitive dye and a reproducible stimulation of the fura-2 signal by the cholinergic agonist, carbachol. A depolarisation-induced increase in the intracellular Ca2+ concentration ([Ca2+]i) was induced by superfusion with 35 mmol l(-1) KCl. This increase in [Ca2+]i was sensitive to Ni2+ and Co2+ as well as omega-conotoxin MVIIA, omega-agatoxin IVA, and SNX-482. The strongest inhibition was achieved by nifedipine (5 x 10(-7) mol l(-1)) and omega-conotoxin GVIA (4.3 x 10(-7) mol l(-1)). These two blockers also inhibited the [Ca2+]i increase evoked by nicotinic receptor stimulation. Consequently, isolated myenteric ganglia in culture express different types of voltage-dependent Ca2+ channels, from which the L- and the N-type seem to be the most important. When exposed to mediators of inflammation such as tumor necrosis factor-alpha (TNF-alpha) or different prostaglandins, no pronounced alterations in the fura-2 ratio were observed suggesting that changes in the Ca2+-signalling are not centrally involved in the response of enteric ganglionic cells to these paracrine substances.

Animals↗

PubMed1989

Human myenteric plexus: confirmation of unfamiliar structures in adults and neonates.

To define the myenteric plexus along the human gastrointestinal tract, we studied three neonatal and six adult specimens, postmortem, by silver impregnation. There were no clear differences between the neonatal and the adult gastrointestinal tracts. In the body of the esophagus, the plexus was sparse, with few ganglia; 30%-40% of fascicular intersections were devoid of ganglia. In the lower 5 cm, the esophagus had thick bundles of nerve fibers ("shunt fascicles"), which crossed the gastroesophageal junction and radiated to the periphery of the stomach through several branches. The plexus in the stomach was uniform, with intermediate and intrafascicular ganglia. A thick nerve bundle encircled the pylorus and gave branches on either side to the antrum and the duodenum. Shunt fascicles in the stomach did not cross the pylorus but extended to the distal antrum. In the duodenum and proximal jejunum, the plexus was regular, but in the mid-small intestine, the longitudinal interganglionic fascicles were more prominent than the circumferential fascicles. Distally, this pattern was reversed; circumferential fascicles were more prominent and ganglia were dense in the terminal ileum. Thin, short shunt fascicles were scattered along the entire small intestine, becoming more abundant in the terminal ileum. Short, thick shunt fascicles traveled proximally from the ileocecal junction for about 25-30 cm. As in the stomach, shunt fascicles did not cross the ileocecal junction, but a thick nerve bundle encircled it. In the cecum and proximal colon, the plexus was sparse with large intermediate and intrafascicular ganglia. In the rectum and distal colon, the plexus was dense, with parafascicular and intrafascicular ganglia. Long ascending nerves extended from the distal rectum into the midcolon. In addition, there were short, thick nerve bundles in the rectum that traveled proximally.

Adult↗

PubMed1991

Determination of levels of cyclic AMP in the myenteric plexus of guinea-pig small intestine.

Enzymatically dissociated ganglia from the myenteric plexus of the guinea-pig small intestine were used to investigate changes in levels of cyclic 3',5'-adenosine monophosphate (cAMP) in response to stimulation of adenylate cyclase by forskolin and inhibition of phosphodiesterase by 3-isobutyl-1-methylxanthine (IBMX). A linear relation with a positive correlation coefficient greater than 0.98 was found between: (1) amount of cAMP and number of ganglia; (2) amount of protein and number of ganglia; (3) amount of DNA and amount of protein; (4) amount of DNA and number of ganglia. Basal levels of cAMP were 2.25 +/- 0.21 fmol per ganglion for 900 ganglia. Forskolin stimulated a dose-dependent increase in cAMP over a concentration range of 0.05 to 50 microM, with a level of 18.6 +/- 4.9 fmol/ganglion at 50 microM forskolin. The inactive forskolin analog 1,9-dideoxyforskolin did not elevate cAMP. Addition of IBMX to the incubation medium stimulated a dose-dependent increase in cAMP over a concentration range of 0.1-1000 microM, with a level of 17.58 +/- 3.38 fmol/ganglion at 1000 microM IBMX. Application of 1 mM IBMX strongly potentiated the stimulating action of forskolin on cAMP levels. Our results derived from direct determination of cAMP changes in small intestinal myenteric ganglia are consistent with existing electrophysiological evidence for second messenger function of cAMP in slow synaptic modulation of excitability in AH/Type 2 neurons of the enteric nervous system.

1-Methyl-3-isobutylxanthine↗

PubMed1986

A rapid silver-free method for staining the myenteric plexus.

A method is presented for the relatively rapid demonstration of the myenteric plexus. Saturated Sudan black B in 70% ethanol followed by 0.01% aqueous buffered thionein were used on intestinal peels (whole-mounts) to stain myelinated and unmyelinated fibers and neuron cell bodies, respectively. In contrast to accepted silver methods, these two kinds of fibers were distinguished clearly; Schwann cell nuclei and nodes of Ranvier were visible. Preparations had the following attributes: relatively low optical density coupled with high visual contrast, freedom from metallic "mirroring," low background staining of subjacent muscle fibers, and presentation of a polychromatic picture. The entire procedure was under the complete and repeatable control of the operator. Perikaryon and nuclear morphology were clearly demonstrated. The limitations of this method are that it does not provide good visualization of individual unmyelinated neuronal processes and does not permit preparation of permanent slides.

Animals↗

PubMed1994

Progressive reorganization of the myenteric plexus during one year following reanastomosis of the ileum of the guinea pig.

The enteric nervous system appears to play a pivotal role in the functional recovery of the gastrointestinal tract after partial resection and reanastomosis, but the structural changes following surgery are not fully understood. The present study was designed to clarify the processes of myenteric plexus regeneration up to one year after transection and reanastomosis of the ileum of the guinea pig. The following techniques were used: nicotinamide adenine dinucleotide (NADH) diaphorase histochemistry, immunostaining of neuron-specific enolase (NSE) in whole-mount preparations, and transmission electron microscopy. Two months after transection and reanastomosis, myenteric ganglion cells with NADH diaphorase reactions were scarce in the center of the lesion, and were less numerous in adjacent areas (3 mm in width) than in the control ileum. In the areas adjacent to the lesion, a few large extraganglionic neurons that did not completely compensate for the loss of ganglion neurons were observed. The remaining ileum showed no changes in NADH diaphorase staining pattern at this stage. Two to 12 months after transection and reanastomosis, ectopic large neurons gradually increased in number not only in the areas adjacent to the lesion but also in part of the remaining ileum, up to 10 cm from the lesion. Concomitantly, large ganglion neurons decreased in number in these areas. In other ileal regions (more than 10 cm distant from the site of transection), no obvious changes in NADH diaphorase staining were noted throughout the observation period. The outgrowth of NSE-containing nerve fibers from the severed stumps was seen two weeks after transection. Six weeks later, numerous bundles of fine nerve fibers with NSE were shown to interconnect the oral and anal cut ends of the myenteric plexus, but they exhibited no subsequent alterations. Transmission electron microscopy revealed that regenerating nerve fiber bundles appeared initially among irregularly arranged smooth muscle cells eight weeks after the operation, as expected from light-microscopic observations. These findings suggest that myenteric ganglion cell bodies, unlike myenteric nerve fibers, require a longer term of reconstruction than previously believed after transection and reanastomosis of the ileum of the guinea pig.

Animals↗

PubMed1973

Intracellular recording from the myenteric plexus of the guinea-pig ileum.

1. Ganglion cells of the myenteric plexus of the guinea-pig ileum have been studied with intracellular micro-electrodes.2. Three types of cell were distinguished. Type 1 cells had a high resistance (58 MOmega) and had properties similar to guinea-pig sympathetic ganglion cells. Type 2 cells were also excitable but had a lower resistance (21 MOmega) and showed accommodation to depolarizing current pulses. Type 3 cells were inexcitable.3. Point stimulation within 150 mum excited neurones either antidromically or orthodromically, sometimes both.4. Antidromic responses had a small all-or-nothing component which was subthreshold for the soma spike. Two or more such components sometimes occurred, and were probably due to stimulation of two or more cell processes.5. Excitatory post-synaptic potentials (e.p.s.p.s) were blocked by hexamethonium (400 muM). They progressively declined in amplitude when elicited at frequencies of 0.05 Hz or more, and this is discussed in relation to studies on acetylcholine (ACh) output.6. Many cells often showed a slow after-hyperpolarization following a direct or antidromic spike. Its mechanism and significance are discussed.7. Spontaneous e.p.s.p.s and spikes were occasionally seen.8. Intracellular injection of a fluorescent dye reveals that the neurones have one to seven processes, which usually arise from the poles of the oval soma.

Acetylcholine↗

PubMed1989

Demonstration of GABA-like immunoreactivity in myenteric plexus of frog stomach.

The GABAergic innervation of the frog stomach was studied by means of an indirect immunohistochemical method. Whole mount preparations were obtained from frog stomachs after the animals had been perfused with a mixture of picric acid, glutaraldehyde and glacial acetic acid. Samples were incubated with an antiserum specific for GABA coupled to BSA with glutaraldehyde. Anti-rabbit IgG-HRP was processed by the two step method (Eckert and Ude 1983). GABA-positive varicose fibers and also nerve cell bodies were revealed within the myenteric plexus. The density of GABA-immunoreactive neurons was not higher than 4-8 cell/cm2, which is approximately 1% of the total nerve cell number in the myenteric plexus.

Animals↗

PubMedDate not supplied

Physiological analysis of delta opioid receptors in the guinea pig myenteric plexus.

Ilea taken from guinea pigs that had been chronically exposed to morphine exhibit a greater tolerance to morphine and normorphine than to the opioid peptides D-ala2-D-leu5-enkephalin (DADLE) or D-met2-pro5-enkephalinamide (DMPE). This differential tolerance strongly implies the existence of at least two different types of opioid receptor in the guinea pig myenteric plexus or two different mechanisms of interaction between opioids and their receptor complex. Since DADLE is considered to be the prototypic ligand for the delta receptor, the above results imply the presence of delta receptors in the guinea pig myenteric plexus and furthermore, that this subtype of opioid receptor is associated with the modulation of release of enteric acetylcholine.

Animals↗

PubMed1997

Human newborn and adult myenteric plexus grows in different patterns.

Whilst embedded within the gut wall the inaccessibility of the enteric nervous system (ENS) is a major drawback for the establishment of an in vitro model for the human ENS. Using a method which combines collagenase digestion, mechanical agitation and manual dissection it was possible to dissect myenteric plexus from human colon of patients at all ages, from newborn to old-age. While complex networks of ganglia and their interconnecting strands could be isolated from newborn gut, the adult tissue allowed only single or small groups of ganglia to be dissected coherently. Pieces of plexus were cultivated on glass coverslips or on plastic sheets respectively. Explants from newborn or older patients displayed different growth patterns. The cytological behaviour of the newborn explants is characterized by an intensive neurite outgrowth. After 1 to 2 days in culture, glial cells start to leave the explant while proliferating and forming a dense cellular carpet. The axons appear partly arranged in bundles, expanding above the glial carpet. Single neurites can leave the carpet and attach directly on the substrate. Semithin sections and EM studies reveal the existence of numerous neurons within the ganglia. The characteristic dense arrangement of neurons, glial cells and neuropil of the myenteric ganglia in vivo was only partly conserved in newborns while in cultured adult ganglia the cells were sparsely scattered throughout the explant with large clefts between the single cells. The ganglia of the adults do not show any considerable neurite outgrowth, which correlates with the low amount of neurons within the ganglia. The migratory behaviour of the adult glial cells is rather moderate, also the proliferation rate compared to the newborn cultures. In general single cells leave the explant without forming an glial carpet as seen in the newborn cultures. The described method delivers an in vitro paradigm for the study of human myenteric plexus. It underlines the differences in growth pattern, neurite outgrowth and glial proliferation from newborn and older children, as well as from adult patients, thus establishing a base line for future studies.

Adolescent↗

PubMed1996

Inhibition of Na+,K+-ATPase by ouabain opens calcium channels coupled to acetylcholine release in guinea pig myenteric plexus.

Ouabain, an Na+K+ATPase inhibitor, increases the release of acetylcholine (ACh) from various preparations in a Ca2+ -independent way. However, in other preparations the release of ACh evoked by ouabain is dependent on the presence of extracellular calcium. In the present study, we have labeled the ACh of myenteric plexus longitudinal muscles of guinea pig ileum and compared the effect of calcium channel blockers on ouabain-evoked release of [3H]ACh. Release of [3H]ACh evoked by ouabain is dose dependent and decreased markedly in the absence of calcium or in the presence of cadmium, a nonspecific calcium channel blocker. N-type calcium channel blockage by the omega-conotoxins GVIA (selective N-type calcium channel blocker) and MVIC (a nonselective calcium channel blocker) inhibited by 45 and 55%, respectively, the release of [3H]ACh. L-type calcium channel suppression by low concentrations of verapamil, nifedipine, and diltiazem had no effect on the release of [3H]ACh. The release of transmitter was also not affected significantly by nickel, a T-type calcium channel blocker. In addition, omega-agatoxin-IVA, at concentrations that block P- and Q-type calcium channels, did not affect significantly the release of [3H]ACh. Thus, extracellular Ca2+ is essential for the release of ACh induced by ouabain from guinea pig ileum myenteric plexus. In this preparation, the N-type calcium channel plays a dominant role in transmitter release evoked by inhibition of Na+K+-ATPase, but other routes of calcium entry in addition to these channels can also support the release of neurotransmitter induced by ouabain.

Acetylcholine↗

PubMed1997

Adenosine 3',5'-cyclic monophosphate-stimulated Ca++ efflux and acetylcholine release in ileal myenteric plexus are mediated by N-type Ca++ channels: inhibition by the kappa opioid receptor agonist.

Adenosine 3',5'-cyclic monophosphate (cAMP) is an important second messenger involved in cholinergic transmission. The aims of this study were to characterize the calcium channels associated with cyclic AMP-mediated acetylcholine release and Ca++ efflux in ileal myenteric plexus. We also examined if this process can be inhibited by agents such as opioids that inhibit N-type calcium channels via a pertussis toxin-sensitive G protein. Application of a cell permeant analogue, 8-bromoadenosine cyclic AMP (8Br-cAMP) (1 mM), and an activator of the adenylyl cyclase system, forskolin (0.1 mM), in a superfusion system resulted in both Ca++ efflux and 3H-acetylcholine (ACh) release from the dispersed myenteric ganglia. A preferential N-type Ca++ channel blocker, omega-Conotoxin GVIA (omega-CgTx, 10-100 nM), significantly inhibited 3H-ACh release stimulated by 8Br-cAMP. 10 nM omega-CgTx also totally inhibited 8Br-cAMP-induced Ca++ efflux, whereas the L-type Ca++ channel blocker, nifedipine (1 microM), and the T-type Ca++ channel blocker, nickel (100 microM), both had no effects on the action of 8Br-cAMP. 3H-ACh release during 0.1 mM forskolin stimulation was inhibited by pretreatment with a kappa receptor agonist, U50488H at 1 to 100 nM. In addition, U50488H significantly inhibited 3H-Ach release and Ca++ efflux elicited by 8Br-cAMP. Inhibition of 3H-ACh release by U50488H was reversed by 3 hr pretreatment with 300 ng/ml pertussis toxin. These results suggest that, in the myenteric plexus, cyclic AMP-stimulated Ca++ efflux and Ach release were mediated by N-type calcium channels. This process may be inhibited by activation of the kappa opioid receptor through pertussis toxin-sensitive G protein(s).

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed2002

Neuronal and glial localization of GABA transporter immunoreactivity in the myenteric plexus.

The neurotransmitter gamma-aminobutyric acid (GABA) is removed from the extracellular space by sodium and chloride dependent high affinity plasma membrane transporters. In the rat central nervous system, three GABA transporters, GAT1, GAT2 and GAT3, have been cloned and localized by immunohistochemistry. The purpose of this study was to examine the distribution of these transporters within the myenteric plexus of the rat gastrointestinal tract. We investigated their cellular locations using GAT1-3 specific antisera in lightly fixed segments of rat duodenum, ileum and colon. Immunohistochemistry revealed a large number of GAT2-immunoreactive structures that surrounded neurons within each ganglion of the myenteric plexus. GAT2 was colocalized in these structures with the glial cell marker p75(NTR), suggesting that the predominant high affinity GABA transporter within enteric glia is GAT2. GAT3 immunoreactivity was localized within many nerve cell bodies, and no labeling for GAT1 was detected, although it was present in retina, which was used as a control. Double labeling for calretinin and nitric oxide synthase (NOS) revealed colocalization of GAT3 with approximately 75% of calretinin-immunoreactive neurons and 15% of NOS-immunoreactive neurons. This suggests that a small proportion of inhibitory motor neurons and at least some putative intrinsic primary afferent neurons within the rat gastrointestinal tract express GAT3. Thus NOS neurons, which appear to utilize GABA as a transmitter, and calretinin-immunoreactive neurons, which do not appear to be GABAergic, both express immunoreactivity for GABA transporters.

Animals↗

PubMed1997

Reduced vagal sensory innervation of the small intestinal myenteric plexus following capsaicin treatment of adult rats.

To determine whether capsaicin treatment damages small intestinal vagal sensory nerve endings, we made intra-nodose injections of wheat-germ agglutinin-horseradish peroxidase conjugate (WGA-HRP) to label peripheral and central vagal endings in control and capsaicin-treated rats. Labeled intraganglionic laminar endings (IGLEs), characteristic of vagal sensory endings of the myenteric plexus, were counted. In controls IGLEs were numerous in the duodenum, less numerous in the jejunum and scarce in the ileum. In capsaicin-treated rats, IGLEs were significantly diminished in all areas of the small intestine. Capsaicin also reduced WGA-HRP activity in the medial and commissural nucleus of the solitary tract. Systemic capsaicin produces a long-lasting loss of vagal IGLEs in the small intestinal myenteric plexus. Such loss is consistent with capsaicin-induced impairment of intestinal reflexes and controls of food intake.

Analysis of Variance↗

PubMed1992

Immunohistochemical reactivity of neuropeptides in plastic-embedded semithin sections of the myenteric plexus in infantile hypertrophic pylorus stenosis.

Pyloric biopsies obtained at pyloromyotomy from 46 infants were studied by light and electron microscopy and compared to 8 autopsy control cases without any evidence of infantile hypertrophic pyloric stenosis (IHPS). A positive family history of this disorder was recorded in 8 cases (2 girls and 6 boys). The most frequent changes in the myenteric plexus comprised axonal alterations. In glial cells, cytoplasmic vacuolisation or an increase of intermediate filaments occurred. In ganglion cells, vacuolisation of perikaryal cytoplasm or dense bodies were observed. No obvious differences were seen between sporadic and hereditary cases. In addition to these fine structural alterations, immunohistochemistry in 6 IHPS cases and 4 controls revealed differences in the distribution of substance P, bombesin, calcitonin gene related peptide and enkephalin-like immunoreactivity within the myenteric plexus between IHPS and control cases. The immunoreactivity, however, was unevenly distributed from case to case and even within individual cases. The reduction of immunoreactivity corresponded, at least in part, to an increase of neurofilaments or abnormal organelles within axons. Increased immunoreactivity was apparently related to focal accumulation of dense cored vesicles noted in the preceding study. It is suggested that these and other changes reported interfere with the normal gastrointestinal reflex mechanisms leading to intestinal obstruction.

Female↗

PubMed1993

Structure of the tertiary component of the myenteric plexus in the guinea-pig small intestine.

The tertiary component of the myenteric plexus consists of interlacing fine nerve fibre bundles that run between its principal ganglia and connecting nerve strands. It was revealed by zinc iodide-osmium impregnation and substance P immunohistochemistry at the light-microscope level. The plexus was situated against the inner face of the longitudinal muscle and was present along the length of the small intestine at a density that did not vary markedly from proximal to distal. Nerve bundles did not appear to be present in the longitudinal muscle as judged by light microscopy, although numerous fibre bundles were encountered within the circular muscle layer. At the ultrastructural level, nerve fibre bundles of the tertiary plexus were found in grooves formed by the innermost layer of longitudinal smooth muscle cells. In the distal parts of the small intestine, some of these nerve fibre bundles occasionally penetrated the longitudinal muscle coat. Vesiculated profiles in nerve fibre bundles of the tertiary plexus contained variable proportions of small clear and large granular vesicles; they often approached to within 50-200 nm of the longitudinal smooth muscle cells. Fibroblast-like cells lay between strands of the tertiary plexus and the circular muscle but were never intercalated between nerve fibre varicosities and the longitudinal muscle. These anatomical relationships are consistent with the tertiary plexus being the major site of neurotransmission to the longitudinal muscle of the guinea-pig small intestine.

Animals↗

PubMed2003

Regeneration of myenteric plexus in the mouse colon after experimental denervation with benzalkonium chloride.

Recent reports suggest a far greater plasticity in nerve tissue than previously believed. As the digestive tract is exposed to a variety of insults, this question is relevant to enteric nerves, but little is known about their ability to recover from damage. To address this problem, we ablated the myenteric plexus of the mouse colon with the detergent benzalkonium chloride (BAC) and followed the ensuing morphologic changes for up to 60 days by using light- and electron microscopy. We found that, 2 days after BAC application, the treated area was essentially devoid of intact nerve elements. From day 7, new nerve fibers were observed within the denervated region. This growth progressed until, at days 30-60, newly grown nerve fibers were present in most of this region, and the pattern of muscle innervation was similar to the normal one. At least part of these fibers originated at neurons within intact ganglia surrounding the denervated region. The cross-sectional area of neurons near the denervated region at day 14 was 52% greater than controls. Glial cells were closely associated with the regenerating nerve fibers. From day 14 onward, we observed undifferentiated cells and differentiating neurons in ganglia surrounding the denervated region, and by day 30, new neurons were present in the myenteric region, along with regenerating nerve fibers. We conclude that the myenteric plexus is endowed with a considerable ability of regeneration and plasticity. The results provide evidence for the presence of stem cells and for an adult neurogenesis in this plexus.

Animals↗

PubMed1989

Quantitative assessment of the stage of neuronal maturation in the developing human fetal gut--a new dimension in the pathogenesis of developmental anomalies of the myenteric plexus.

There are two main theories of the normal development of the enteric nervous system: the classical theory suggests that the enteric neuroblasts migrate along the alimentary tract in a single cranio-caudal direction. However, the second theory postulates a dual gradient of neuronal development. The present study aims to support the second theory and contribute to the understanding of the pathogenesis of Hirschsprung's disease and its allied gut motility disorders. Using a histomorphometric method, quantitative estimation of the myenteric intraganglionic neuronal development was made in tissues from various selected levels of the gut in 32 normal human fetuses of 11 to 24 weeks ovulation age. A parallel study with special chromatin staining was carried out from these materials to investigate different neurons in the myenteric plexus. Development of intraganglionic neurons was shown to be more advanced in the esophagus, less so in the rectosigmoid and least so in the ileocecal region: the mean values of neuronal and nuclear volume were found in the esophagus greater than in rectosigmoid and ileocecal region as ovulation age progressed. Intraganglionic mitotic figures were detected at all the selected levels of the gut. A decrease of the mitosis index as age progressed was observed. We showed that myenteric neurons followed a dual gradient of development proceeding from both ends to the middle of the gut in mid-trimester human fetuses. Our findings are compatible with the suggestion that any alterations in the fetal gut microenvironment may affect seriously the normal development of a multipotential precursor cell population resulting in various congenital anomalies of the myenteric plexus.

Cell Differentiation↗