Myenteric Plexus

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The number and profile of reactive NADH-d and NADPH-d neurons of myenteric plexus of six-month-old rats are different in the cecum portions

The number and profile of reactive NADH-d and NADPH-d neurons of myenteric plexus of six-month-old rats are different in the cecum portions

segments, distinguish the regions of material collection (Peng et al. 2001, Molinari et al. 2002, Seyfert 2003). Differences in neuronal density of myenteric plexus from the same intestinal segment were also found in the large intestine of guinea pig (Irwin 1931); rat colon (Barbosa 1973); rat ileum (Miranda-Neto et al. 2001), and human esophagus (De Souza et al. 1988). In guinea pigs, the relative proportion of positive NADPH-d myenteric neurons is higher in the esophagus (54-69%) (Furness et al. 1994, Morikawa & Komuro, 1998) than in the stomach (21%), small intestine (12-19%) and colon (25%) (Furness et al. 1994). The results obtained by Wu et al. (2003) indicate that about 64-89% of the myenteric neurons in esophagus of young and old rats are positive NADPH-d neurons. This proportion is high when compared to other results found in another parts of gastrointestinal tract: 29-38% in stomach (Timmermans et al. 1999); 28% in duodenum (Jarvinen et al. 1999); 15-27% in ileum (Cracco & Filogamo 1994, Cowen et al. 2000) and 12-57% in colon (Nichols et al. 1993).
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Morphometry and acetylcholinesterase activity of the myenteric plexus of the wild mouse Calomys callosus

Morphometry and acetylcholinesterase activity of the myenteric plexus of the wild mouse Calomys callosus

Figure 2 - Stretch preparation from the muscle layer of the esophagus (A), stomach (B), je- junum (C) and colon (D) showing the myenteric plexus. Cholines- terase method. A, Intensely stained neurons (arrows). B-D, The plexus consists of a primary meshwork of thick nerve bundles (arrows) and a secondary mesh- work of finer bundles (arrow- heads). In the primary mesh- work, the nerve cell bodies oc- cur mainly at the nodes of the plexus. Note the variable inten- sity of nerve cell staining. Scale bars = 40 µm.

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Effects of infection with Toxoplasma gondii oocysts on the intestinal wall and the myenteric plexus of chicken (Gallus gallus)

Effects of infection with Toxoplasma gondii oocysts on the intestinal wall and the myenteric plexus of chicken (Gallus gallus)

There are a few studies assessing the hen myenteric plexus. In this experiment, the structure of the myenteric plexus in both groups was similar to what was described by Kuder et al. (2003), formed by ganglions of different sizes and shapes, presenting no modifications as a result of the infection. Quantitative analysis of the myenteric plexus revealed a loss of ~70% of the duodenal neurons. Since methylene blue is a panneural marker, it is deducted that 70% of the total population of myenteric neurons may have been lost, possibly by the direct action of Toxoplasma gondii or indirectly by chemical mediators modulated on the response to the infection. It is known that IFN-ã and nitric oxide (NO) are among the mediators involved on the infection with protozoans and that they may induce to morphological and quantitative changes of the enteric neurons (Arantes et al. 2004). Former studies with rats orally infected with tachyzoites from a Genotype III T. gondii strain demonstrated that there was neither diarrhea nor neuronal death during chronic or acute infection, different from what was observed in this experiment (Sugauara et al. 2008). As this has been an exploratory study, new studies are necessary to clarify whether the neurons were lost of partially redistributed as well as which neuronal subpopulation was mostly impaired. In a former study involving the same hens, the parasite was re-isolated from their brain pool and hearts. From the six infected hens, the parasite was re-isolated in four, with 29.2% of the mice positive serum and the detection of tissue cysts in 71.4% (Galli et al. 2008), what confirms the chronicity of the infection in the birds studied.
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Myenteric plexus is differentially affected by infection with distinct Trypanosoma cruzi strains in Beagle dogs

Myenteric plexus is differentially affected by infection with distinct Trypanosoma cruzi strains in Beagle dogs

The pathogenic mechanisms of digestive lesions are not yet fully understood; however, during the acute phase, neuronal damage could be caused by direct or indirect tissue effects of parasitism and subsequent in- flammatory response in regions close to the enteric ganglia (Köberle & Alcântara 1960, Teixeira et al. 1970, Ribeiro Dos Santos & Hudson 1980, 1981). According to Tafuri (1971), acute enteric nervous system (ENS) changes in digestive ChD are related to organ motor dys- function that results in accumulation of food or faeces in the lumen, which can compress the mucosa and induce dilation and ischemic events. These events, in turn, can cause regressive lesions of the mucosa and an inflam- matory process that reaches the submucosa, leading to submucous plexus injuries and then the muscularis, reaching the myenteric plexus already injured by acute infection. The accumulation and maintenance of the in- flammatory cells throughout the chronic disease are as- sociated with tissue destruction and disease progression to fibrosis, which is one of the factors responsible for modification of the intermuscular interstitium compo- nents. The involvement of the ENS during the course of T. cruzi infection has been shown in many studies using immunohistochemistry techniques with multiple mark- ers and histopathological findings show that the effects are not restricted to neuronal damage, since changes in enteric glial cell (EGC) numbers and phenotype are also observed (da Silveira et al. 2007, 2009, Iantorno et al. 2007). Thus, patients with megaoesophagus and/or megacolon show reductions in neurons (Adad et al. 2001, da Silveira et al. 2005) and nerve fibres (da Silveira et al. 2007), moreover, there is loss of S100 + glial cells (da
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REPOSITORIO INSTITUCIONAL DA UFOP: Myenteric plexus is differentially affected by infection with distinct Trypanosoma cruzi strains in Beagle dogs.

REPOSITORIO INSTITUCIONAL DA UFOP: Myenteric plexus is differentially affected by infection with distinct Trypanosoma cruzi strains in Beagle dogs.

The pathogenic mechanisms of digestive lesions are not yet fully understood; however, during the acute phase, neuronal damage could be caused by direct or indirect tissue effects of parasitism and subsequent in- flammatory response in regions close to the enteric ganglia (Köberle & Alcântara 1960, Teixeira et al. 1970, Ribeiro Dos Santos & Hudson 1980, 1981). According to Tafuri (1971), acute enteric nervous system (ENS) changes in digestive ChD are related to organ motor dys- function that results in accumulation of food or faeces in the lumen, which can compress the mucosa and induce dilation and ischemic events. These events, in turn, can cause regressive lesions of the mucosa and an inflam- matory process that reaches the submucosa, leading to submucous plexus injuries and then the muscularis, reaching the myenteric plexus already injured by acute infection. The accumulation and maintenance of the in- flammatory cells throughout the chronic disease are as- sociated with tissue destruction and disease progression to fibrosis, which is one of the factors responsible for modification of the intermuscular interstitium compo- nents. The involvement of the ENS during the course of T. cruzi infection has been shown in many studies using immunohistochemistry techniques with multiple mark- ers and histopathological findings show that the effects are not restricted to neuronal damage, since changes in enteric glial cell (EGC) numbers and phenotype are also observed (da Silveira et al. 2007, 2009, Iantorno et al. 2007). Thus, patients with megaoesophagus and/or megacolon show reductions in neurons (Adad et al. 2001, da Silveira et al. 2005) and nerve fibres (da Silveira et al. 2007), moreover, there is loss of S100 + glial cells (da
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Effect of the Ascorbic Acid Treatment on the NADHd- Positive Myenteric Neurons of Diabetic Rats Proximal Colon

Effect of the Ascorbic Acid Treatment on the NADHd- Positive Myenteric Neurons of Diabetic Rats Proximal Colon

Morphometric results of the proximal colon No significant difference was observed when comparing the neuronal profile results between the control and diabetic animals groups (p > 0.05). On the other hand, an increase in the cellular profile of the AA-supplemented diabetic animals (17.3 %) was observed when compared to the diabetic animals (p < 0.05) (Fig. 2). Representative micrographs of NADHd-positive neurons of proximal colon in myenteric plexus whole mount from all the animal groups studied are shown in Fig. 3.
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Arq. NeuroPsiquiatr.  vol.58 número4

Arq. NeuroPsiquiatr. vol.58 número4

Taking into account the diabetic complications on sympathetic and parasympathetic divisions of the autonomic nervous system and peripheral nerves, as well as the lack of studies on the morphological abnormalities of the myenteric plexus in rats with induced diabetes, this study aims to evaluate the number and the cytoplasmic basophily of the cell bodies of myenteric neurons in rats with diabetes mellitus induced by streptozotocin, 6 and 19 weeks after its induction.

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Benefits of caloric restriction in the myenteric neuronal plasticity in aging rats

Benefits of caloric restriction in the myenteric neuronal plasticity in aging rats

Aging is a biologic process characterized by progressive damage of structures and functions of organic systems. In gastrointestinal tract, it can involve enteric nervous system, which plays an important role in digestion and absorption of nutrients, causing hastening of intestinal transit thus reducing its absorptive function. Caloric restriction has been used in several studies with the intention of delaying deleterious effects of aging. This study aimed to evaluate the effects of caloric restriction on myenteric neurons of ileum by aging in rats. 30 Wistar rats were grouped as follows: GI (animals aged 6 months fed with normal diet), GII (animals aged 18 months fed with normal diet) and GIII (animals aged 18 months subject to 31% of caloric restriction). The rats of the GI group were euthanized at 6 months of age and after experimental period of 12 months animals of the group GII and GIII were euthanized, the ileum of all groups were collected, measured and processed by NADPH-dp and Acetylcholinesterase. Quantitative analysis of neurons revealed that aging promotes the increasing of myenteric neurons NADPH-dp and reduces Acetylcholinesterase neuronal population. However, in the cellular proile area, were not observed signiicant differences between the groups. The caloric restriction has been eficient and can be used preventively because it minimizes quantitative changes associated with aging on ileum myenteric plexuses. Key words: aging, caloric restriction, myenteric plexus, small intestine.
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Arq. Gastroenterol.  vol.48 número3

Arq. Gastroenterol. vol.48 número3

33. Sant’ana DM, Miranda-Neto MH, de Souza RR, Molinari SL. Morphological and quantitative study of the myenteric plexus of the ascending colon of rats subjected to proteic desnutrition. Arq Neuropsiquiatr. 1997;55:687-95. 34. Schneider LC, Perez GG, Banzi SR, Zanoni JN, Natali MR, Buttow NC. Evaluation

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Hypertrophy of NADH-diaphorase positive myenteric neurons in rat jejunum after acute infection caused by Toxoplasma gondii

Hypertrophy of NADH-diaphorase positive myenteric neurons in rat jejunum after acute infection caused by Toxoplasma gondii

The segments of all animals were submitted to NADH-diaphorase histochemistry to evidence metabolic-active myenteric neurons (13). The jejunum was washed and filled with Krebs solution, immersed in a 0.3% Triton X-100® solution (Sigma, USA) for five minutes and then washed again in Krebs solution. Segments were submersed in a medium containing 0.05 g of β-NADH (Sigma, USA) and 25 mL of nitro blue tetrazolium (0.5 mg/mL) (Sigma, USA) for 45 minutes. The reaction was interrupted with buffered formol. Then, the segments were fixed in 10% buffered formol solution until the microdissection procedure in which the mucosa and submucosa were removed with the aid of a transillumination stereomicroscope to expose the myenteric plexus located in the external muscle. Thus, the whole mounts were dissected in ascending series of ethyl alcohol, diaphanized in xylol and mounted using Permount® (Fisher Scientific, USA).
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Hyperplasia of interstitial cells of cajal in sprouty homolog 4 deficient mice.

Hyperplasia of interstitial cells of cajal in sprouty homolog 4 deficient mice.

S16 Fig. Myenteric plexus area is unaltered in the colon of 3 month old Spry4 KO and Kit WT/K641E. HuC/D-ir highlights soma of myenteric neurons in colon of 3-month-old WT, Spry4 KO and [r]

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Arq. NeuroPsiquiatr.  vol.54 número2

Arq. NeuroPsiquiatr. vol.54 número2

We therefore noted that gaps exist on the literature about different post-undernutrition periods; this fact elicited us to study the neurons of the myenteric plexus of rats whose mother[r]

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Enteric Neuronal Damage, Intramuscular Denervation and Smooth Muscle Phenotype Changes as Mechanisms of Chagasic Megacolon: Evidence from a Long-Term Murine Model of Tripanosoma cruzi Infection.

Enteric Neuronal Damage, Intramuscular Denervation and Smooth Muscle Phenotype Changes as Mechanisms of Chagasic Megacolon: Evidence from a Long-Term Murine Model of Tripanosoma cruzi Infection.

According to Koberle (1968) [45], dilatation and hypertrophy of the colon is initiated when the decrease in the number of ganglion cells exceeds the critical threshold of 55%. Our model also presents an opportunity to prove Koberle’s thesis of the acute-phase neuronal damage responsible for the neuronal loss (approximately 86%) and for the impairment of myenteric nerve function as one of the most likely mechanisms for development of Chagasic megacolon. In our opinion, in addition to the decreased number of neuronal cells in the myenteric plexus, one of our most original results is the significant decrease in the density of the intramuscular innervation (axonal density within the smooth muscle) in the chronic-phase group compared with its control. The activity of the smooth muscle of the GI tract is converted into coordinated peristalsis by the ganglion cells of the Aüerbach's plexus. Disturbance in the peristalsis leading to the lack of coordination of the wave-like forward motion causes stagnation, retention, and dilatation of hollow viscera. Because the distension of the muscle fibers is the primary cause of hypertrophy, continuous dilatation and hypertrophy lead to the well-known mega formations based on the disturbance of the intrinsic innervation of the organ [12,46]. The association between this pathogenetic mechanism and the inflammatory-induced intrinsic denervation can explain the natural history of mega formations in CD.
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Alterations in the duodenum myenteric neurons of Wistar rats after ingesting of 2,4 dichlorophenoxyacetic acid

Alterations in the duodenum myenteric neurons of Wistar rats after ingesting of 2,4 dichlorophenoxyacetic acid

The nitrergic neurons are, among the total neuronal population of the myenteric plexus, responsible for inhibition of digestive tract muscles (FURNESS, LI, YOUNG  et  al., 1994). Nitrergic myenteric neurons can be evidenced by histochemical method of the enzyme nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase) (SCHERER-SINGLER, VINCENT, KIMURA  et  al., 1983). These neurons plays a role in the mechanism of defense against free radicals improving it’s function of producing nitric oxide, which makes them more resistant to adverse conditions that affect other types of enteric neurons (COWEN, JOHNSON, SOUBEYRE et al., 2000).
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Arq. NeuroPsiquiatr.  vol.55 número1

Arq. NeuroPsiquiatr. vol.55 número1

ABSTRACT - We have studied the morphological and quantitative aspects of the myenteric plexus neurons of the proximal colon in rats ( Rattus฀norvegicus of Wistar strain) submitted to a[r]

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Arq. Gastroenterol.  vol.45 número3

Arq. Gastroenterol. vol.45 número3

located in the myenteric plexus and to innervate sensory receptors FIGURE 2. Area under the curve (AUC) of the esophageal contractions of patients with Chagas’ disease (CD, n = 30) and control subjects (CO, n = 44) after wet and dry swallows, measured at 12 and 17 cm from the upper esophageal sphincter. The horizontal bars represent the means. * P <0.05 vs control dry and Chagas’ disease wet and dry

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Brachial plexus variation involving the formation and branches of the cords

Brachial plexus variation involving the formation and branches of the cords

Knowledge of brachial plexus variations has important anatomical and surgical clinical applications especially in relation to trauma and surgical procedures of upper limb [10,11]. The present case report provides additional knowledge on brachial plexus variations to clinicians, which may help to avoid damage during surgical procedures related to plastic and reconstructive surgeries.

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Arq. Gastroenterol.  vol.48 número1

Arq. Gastroenterol. vol.48 número1

duodenum of each animal. Results - After the supplementation with L-glutamine in the duodenum, we observed a preservation of neuronal density in groups normoglycemic and diabetic (P<0.05). We also observed a preservation of the cell bodies area in diabetic animals (group treated with L-glutamine) (P<0.05). In the cecum, that preservation was not evident. Conclusion - Supplementation with L-glutamine (1%) promoted a neuroprotective effect on the myenteric neurons from the duodenum of rats, both in terms of natural aging and of diabetes mellitus.

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Arq. NeuroPsiquiatr.  vol.75 número9

Arq. NeuroPsiquiatr. vol.75 número9

The treatment of complete post-traumatic brachial plexus palsy resulting in a flail shoulder and upper extremity remains a challenge to peripheral nerve surgeons. The option of upper limb amputation is controversial and scarcely discussed in the literature. We believe that elective amputation still has a role in the treatment of select cases. The pros and cons of the procedure should be intensely discussed with the patient by a multidisciplinary team. Better outcomes are usually achieved in active patients who strongly advocate for the procedure. Keywords: brachial plexus neuropathies; amputation; upper extremity; artificial limbs
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Radiol Bras  vol.47 número5

Radiol Bras vol.47 número5

Conclusion: Considering the wide range of abdominal anatomical variations and the characteristics of needle insertion pathways, celiac plexus block should not be standardized. Imaging should be performed prior to the procedure in order to reduce the risks for injuries or for negative outcomes to patients. Gender-related anatomical variations involved in celiac plexus block should be more deeply investigated, since few studies have addressed the subject.

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