Chemical coding of neurons in the myenteric plexus and external muscle of the small and large intestine of the mouse

Sang, Qian; Young, Heather M.

doi:10.1007/s004410050565

Cited by 243 publications

(286 citation statements)

References 57 publications

Supporting

Mentioning

241

Contrasting

Unclassified

Order By: Relevance

“…The estimated cholinergic subpopulation was predominant in our study representing approximately 76% in the control group and 72% in the malnourished group. This finding was also noticed for small intestine which presented 60% of cholinergic neurons (Sang and Young 1996). The estimated number of cholinergic was 6.1% smaller for the malnourished group with a possible eduction of approximately 4.5% of negative NADPH-d neurons (cholinergic).…”

Section: Myenteric Neurons In Malnourished Ratssupporting

confidence: 68%

Characterization of the myenteric neuronal population and subpopulation of the duodenum of adult wistar rat fed with hypoproteic chow

Sant’Ana

Araújo

Ramos

et al. 2012

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

The effects of severe protein malnutrition (4%) on myenteric neurons of Wistar rat duodenum, in relation to a standard 22%-protein diet for rodents, were assessed in this study. Segments of the duodenum from 10 rats from each nutritional group were submitted to the elaboration of whole mounts -5 stained with Giemsa to determine the total population of myenteric neurons and the others stained by a histochemical method to detect nervous cells through the NADPH-diaphorase enzyme activity for studying the subpopulation of nitrergic neurons. The area of 100 neurons per animal, totalizing 2,000 neurons, were randomly measured by using the Image Pro-Plus ® software. Malnourished rats presented 34.38% lower body weight and 10.60% duodenum length reduction when compared to the control group. Quantitative analysis demonstrated no significant differences between control and malnourished group by using Giemsa; however, as the organ reduction was not followed by an increase inversely proportional to the density of neurons, the condition imposed suggests the loss of neurons from the total population. Nevertheless, through NADPH-d histochemistry, there was a neuronal density increase for the malnourished group. There was no significant difference between the groups for both techniques with respect to the morphometric analysis of the body cell.

show abstract

Section: Myenteric Neurons In Malnourished Ratssupporting

confidence: 68%

Characterization of the myenteric neuronal population and subpopulation of the duodenum of adult wistar rat fed with hypoproteic chow

Sant’Ana

Araújo

Ramos

et al. 2012

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

show abstract

“…7 Among the substances that have been localized in enteric neurons somata are vasoactive intestinal peptide, nitric oxide, 20 somatostatin, tachykinins (substance P), 21 calcitonin gene-related peptide, enkephalin, neurotensin, gastrin, [22][23][24] galanin, 25 and ␥-aminobutyric acid transaminase. 26 The measurements of the neuron areas in the two groups (control and infected) and the significant difference between them suggest that there is a preferential loss of a particular size category, with some types of neurons being susceptible.…”

Section: Discussionmentioning

confidence: 99%

Morphometry and acetylcholinesterase activity of the myenteric neurons of the mouse colon in the chronic phase of experimental Trypanosoma cruzi infection.

Maifrino¹,

Liberti²,

Watanabe³

et al. 1999

The American Journal of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

Abstract. The myenteric plexus of the proximal colon, midcolon, and distal colon was studied in mice chronically infected with the Y strain of Trypanosoma cruzi by means of histochemical methods for NADH-diaphorase and acetylcholinesterase (AChE) on whole mount preparations. Ganglia of infected mice displayed an irregular distribution, with neurons severely altered in form and were found side by side with slightly degenerated or morphologically normal ones. Significant reductions of at least 36% in the numbers of neurons were recorded in all regions of the colons of infected animals, especially in the distal colon where the neuron number decreased by more than 44%. Measurements of neuron size suggest that the neuronal destruction caused by T. cruzi affected the medium and large neurons. The small neurons apparently were not affected by the infection. The histochemical demonstration of AChE by the direct coloring copper ferrocyanide method showed that in the control animals, most of the neurons of the plexus displayed AChE activity in the cytoplasm although the neurons showed different reaction intensities. The AChE activity was also present, but at a lower intensity, in the myenteric plexus of the colons of infected animals. These results suggest that the T. cruzi infection affects some categories of neurons and implies that some particular enteric neurotransmitter systems could be affected and the potency of their action upon intestinal function consequently reduced.The digestive form of Chagas' disease involves denervation of the myenteric plexus, which influences disturbances of motility and absorption. 1 The extent of the neurolysis will determine the severity of the sequelae and the patient's future degree of clinical adaptation. 2 Studies involving the myenteric plexus of the colon of animals chronically infected with Trypanosoma cruzi have been carried out and have demonstrated a reduction of 34-37% of the neuronal population. 3,4 Okumura 5 found that 65% of the ganglion neurons of the mouse colon may be destroyed in experimentally infected mice. These studies were done in histologic sections made in the plane of the plexus. However, these sections rarely pass through more than a few ganglia simultaneously, while whole mount preparations, in which the muscle layers are stretched on a plane, can display the whole plexus. 6 Furthermore, the use of whole mount preparations presents the myenteric plexus as a monolayer of nerve cells, and it has therefore been possible, in parallel with neuron counts, to make measurements of neuron somata of unsectioned nerve cells. 7 Therefore, in this study, we used laminar preparations of the mouse colon to 1) quantify the loss of myenteric neurons that occurred with T. cruzi infection, 2) see whether any particular size grouping of neurons is affected, and 3) determine the activity of acetylcholinesterase (AChE) in the myenteric plexus of the mouse colon chronically infected with T. cruzi. MATERIALS AND METHODSTwenty male Swiss mice weighing 20-25 g (13-15 weeks old) were ...

show abstract

“…The ENS is derived from vagal and sacral enteric neural crest cells (ENCs), which invade the foregut and hindgut, respectively (2,3). Once situated within the gut, ENCs migrate along the developing bowel, proliferate, and differentiate to form many different neuronal subtypes and make synaptic connections (4,5). Migration of ENCs within the gut requires signaling between these cells and the gut environment and depends on dynamic changes in cell shape and adhesive properties.…”

mentioning

confidence: 99%

Expression profiling the developing mammalian enteric nervous system identifies marker and candidate Hirschsprung disease genes

Heanue

Pachnis

2006

Proc. Natl. Acad. Sci. U.S.A.

106

121

View full text Add to dashboard Cite

The enteric nervous system (ENS) is composed of neurons and glial cells, organized as interconnected ganglia within the gut wall, which controls persistalsis of the gut wall and secretions from its glands. The Ret receptor tyrosine kinase is expressed throughout enteric neurogenesis and is required for normal ENS development; humans with mutations in the RET locus have Hirschsprung disease (HSCR, an absence of ganglia in the colon), and mice lacking Ret have total intestinal aganglionosis. The Ret mutant mouse provides a tool for identifying genes implicated in development of the ENS. By using RNA from WT and Ret mutant (aganglionic) gut tissue and DNA microarrays, we have conducted a differential screen for ENS-expressed genes and have identified hundreds of candidate ENS-expressed genes. Forty-seven genes were selected for further analysis, representing diverse functional classes. We show that all of the analyzed genes are expressed in the ENS and that the screen was sensitive enough to identify genes marking only subpopulations of ENS cells. Our screen, therefore, was reliable and sensitive and has identified many previously undescribed genes for studying ENS development. Moreover, two of the genes identified in our screen Arhgef3 and Ctnnal1, have human homologues that map to previously identified HSCR susceptibility loci, thus representing excellent candidates for HSCR genes. This comprehensive profile of ENS gene expression refines our understanding of ENS development and serves as a resource for future developmental, biochemical, and human genetic studies.T he enteric nervous system (ENS) is composed of a vast number of neurons and glial cells, which form interconnected ganglia that control the contractility of the smooth muscle of the gut wall and the secretory activity of its glands (1). The ENS is derived from vagal and sacral enteric neural crest cells (ENCs), which invade the foregut and hindgut, respectively (2, 3). Once situated within the gut, ENCs migrate along the developing bowel, proliferate, and differentiate to form many different neuronal subtypes and make synaptic connections (4, 5). Migration of ENCs within the gut requires signaling between these cells and the gut environment and depends on dynamic changes in cell shape and adhesive properties. How cell shape and adhesion are controlled to allow regulated and directed migration of ENCs currently is unknown. Furthermore, how cell fate decisions are controlled to specify the correct number and subtypes of neurons and glial cells within ENS ganglia or how correct synaptic circuits are established also is unknown.Genetic studies in mouse and human have identified several genes whose function is required for normal ENS development (6, 7). For example, the Ret receptor tyrosine kinase is expressed in ENCs during migration into the gut and persists during later ENS development (8). Humans carrying mutations in RET develop congenital megacolon [Hirschsprung disease (HSCR) OMIM 142623; ref. 7], which is characterized by the absence of enteric ga...

show abstract

Chemical coding of neurons in the myenteric plexus and external muscle of the small and large intestine of the mouse

Cited by 243 publications

References 57 publications

Characterization of the myenteric neuronal population and subpopulation of the duodenum of adult wistar rat fed with hypoproteic chow

Characterization of the myenteric neuronal population and subpopulation of the duodenum of adult wistar rat fed with hypoproteic chow

Morphometry and acetylcholinesterase activity of the myenteric neurons of the mouse colon in the chronic phase of experimental Trypanosoma cruzi infection.

Expression profiling the developing mammalian enteric nervous system identifies marker and candidate Hirschsprung disease genes

Contact Info

Product

Resources

About