Projections of chemically identified myenteric neurons of the small and large intestine of the mouse

Sang, Qian; Williamson, Susan; Young, Heather M.

doi:10.1046/j.1469-7580.1997.19020209.x

Cited by 93 publications

(98 citation statements)

References 53 publications

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“…Quantitative analysis at P30 demonstrated Cre-dependent EYFP expression in 100% of SOX10 + enteric glia, 62% of distal small bowel myenteric neurons, 17% of colon myenteric neurons, 93% of distal small bowel nNOS-expressing myenteric neurons, 90% of distal small bowel calretinin + myenteric neurons, 76% of colon nNOS + myenteric neurons, and 80% of colon calretinin + myenteric neurons (Supplemental Figure 5). We also noted that, in our mice, 12% of colon myenteric neurons had nNOS immunoreactivity and 12% had calretinin immunoreactivity, lower percentages than previously reported in BALB/c mice (25). Finally, we performed immunohistochemistry for PHOX2B in these mice at E10.5 and E11.5 (Supplemental Figure 6) and found that Cre-induced recombination occurred with some, but not all, ENS precursors by E10.5 and in almost all ENS precursors by E11.5.…”

Section: Rb1 Loss In the Ens Causes A Severe Intestinal Motility Disocontrasting

confidence: 44%

Retinoblastoma protein prevents enteric nervous system defects and intestinal pseudo-obstruction

Fu¹,

Landreville

Agapova

et al. 2013

J. Clin. Invest.

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The retinoblastoma 1 (RB1) tumor suppressor is a critical regulator of cell cycle progression and development. To investigate the role of RB1 in neural crest-derived melanocytes, we bred mice with a floxed Rb1 allele with mice expressing Cre from the tyrosinase (Tyr) promoter. TyrCre + ;Rb1 fl/fl mice exhibited no melanocyte defects but died unexpectedly early with intestinal obstruction, striking defects in the enteric nervous system (ENS), and abnormal intestinal motility. Cre-induced DNA recombination occurred in all enteric glia and most small bowel myenteric neurons, yet phenotypic effects of Rb1 loss were cell-type specific. Enteric glia were twice as abundant in mutant mice compared with those in control animals, while myenteric neuron number was normal. Most myenteric neurons also appeared normal in size, but NO-producing myenteric neurons developed very large nuclei as a result of DNA replication without cell division (i.e., endoreplication). Parallel studies in vitro found that exogenous NO and Rb1 shRNA increased ENS precursor DNA replication and nuclear size. The large, irregularly shaped nuclei in NO-producing neurons were remarkably similar to those in progeria, an early-onset aging disorder that has been linked to RB1 dysfunction. These findings reveal a role for RB1 in the ENS. IntroductionChronic intestinal pseudo-obstruction (CIPO) is the clinical indication for 9 percent of small bowel transplants (1), yet the etiology for these disorders remains poorly understood. CIPO is diagnosed when bowel motility defects cause functional, but not mechanical, obstruction, leading to abdominal distension, pain, malnutrition, and, in severe cases, dependence on parenteral nutrition or intestinal transplantation for survival. It is likely that diverse genetic, infectious, autoimmune, metabolic, and toxic insults all contribute to CIPO etiology.Intestinal motility and many other aspects of bowel function are controlled by an interconnected intrinsic network of neurons and glia called the enteric nervous system (ENS) (2-4). The ENS forms from neural crest-derived cells that migrate through fetal bowel, proliferate extensively, and then exit the cell cycle and differentiate into many different neuronal subtypes (5-7). Defects in specific types of enteric neurons may cause life-threatening disease, and, like in the central nervous system, neurons in the ENS must be present in the proper ratios and with correct patterning for the bowel to work well. Signals that control ENS precursor proliferation and cell cycle exit are incompletely understood. Furthermore, the ENS can be damaged in many ways, often with preferential effects on NO-producing enteric neurons that inhibit bowel contraction (8). There are also regional differences in the susceptibility of enteric neurons to damage that are not well understood (9).We initially intended to develop a model of melanoma by deleting the tumor suppressor retinoblastoma 1 (Rb1) in melanocytes,

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Section: Rb1 Loss In the Ens Causes A Severe Intestinal Motility Disocontrasting

confidence: 44%

Retinoblastoma protein prevents enteric nervous system defects and intestinal pseudo-obstruction

Fu¹,

Landreville

Agapova

et al. 2013

J. Clin. Invest.

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“…Neural activity also influences differentiation, as (106). Studies using myotomy and myectomy followed by immunohistochemistry demonstrate that excitatory motor neuron axons project rostrally, while inhibitory motor neurons project caudally within the longitudinal axis of the myenteric plexus before entering circular or longitudinal muscle (106,107). Elegant models of enteric neuron circuitry now exist based on decades of work (1,22,(108)(109)(110), but mechanisms needed to establish these connections remain obscure.…”

Section: Ens Morphogenesis Does Not End When Encdcs Reach "The End"mentioning

confidence: 99%

Building a second brain in the bowel

Avetisyan¹,

Schill²,

Heuckeroth³

2015

J. Clin. Invest.

114

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“…Descriptions found on the literature assess several aspects of this subdivision of the autonomic nervous system [1][2][3][4][5] and reveal the richness of structure and organization of this neuronal population of magnitude similar to that of the spinal 6 . Systematization of the studies on the enteric neurons, especially those of the myenteric plexus of species such as the rat, mouse and guinea-pig, have permitted to determine, with relative precision, the functions of specific groups of neurons [7][8][9] . Due to the accessibility of the ENS, investigations about the alterations caused by pathophysiological states, such as diabetes, have been equally productive; there are reports on the literature [10][11][12][13] about the differential effects of diabetes on specific neurotransmitter systems and on neurons of diverse intestinal segments.…”

Section: Palavras-chave: Duodeno Neurônios Mientéricos Diabetes Agumentioning

confidence: 99%

Number and size of myenteric neurons of the duodenum of adult rats with acute diabetes

Furlan

Miranda-Neto

Sant’Ana

et al. 1999

Arq. Neuro-Psiquiatr.

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-This study had as its purpose to assess the effects of acute diabetes induced by streptozotocin (35 mg/kg body weight) on the number and size of the myenteric neurons of the duodenum of adult rats considering equally the antimesenteric and intermediate regions of the intestinal circumference. Experimental period extended for a week. Neuronal counts were carried out on the same number of fields of both regions of the duodenal circumference and measurements of neuronal and nuclear areas on equal numbers of cells. Number and size of the myenteric neurons stained with Giemsa were not significantly different between groups. On the other hand, the proportion of NADH-positive neurons increased from 18.54% on the controls to 39.33% on the diabetics. The authors discuss that this increased reactivity probably results from a greater NADH/NAD + ratio, described in many tissues of diabetic animals, which has consequences on the modulation of the enzymes that use these cofactors and whose activity is detected by the NADH-diaphorase technique.KEY WORDS: duodenum, myenteric neurons, acute diabetes, NADH-diaphorase.Número e tamanho dos neurônios mientéricos do duodeno de ratos adultos com diabetes agudo RESUMO -Este estudo teve como objetivo avaliar os efeitos do diabetes agudo induzido por estreptozootocina (35 mg/kg de peso corporal) sobre o número e tamanho dos neurônios mientéricos do duodeno de ratos adultos considerando de forma equivalente as regiões antimesentérica e intermediária da circunferência intestinal. O período experimental se estendeu por uma semana. As contagens neuronais foram feitas em igual número de campos nas duas regiões da circunferência duodenal e as mensurações das áreas neuronais e nucleares em igual número de células. O número e o tamanho dos neurônios corados por Giemsa não foram significativamente diferentes entre os grupos. Por outro lado, a proporção de neurônios NADH-positivos aumentou de 18,54% nos animais controles para 39,33% nos diabéticos. Os autores discutem que essa maior reatividade possivelmente resultou do aumento da proporção NADH/NAD + , descrita em diversos tecidos de animais diabéticos, que repercute na modulação das enzimas que utilizam esses cofatores e cuja atividade é detectada pela técnica da NADHdiaforase. PALAVRAS-CHAVE: duodeno, neurônios mientéricos, diabetes agudo, NADH-diaforaseThe knowledge about the mammalian enteric nervous system (ENS) can be considered, currently, as wide and in some instances, quite deep. Descriptions found on the literature assess several aspects of this subdivision of the autonomic nervous system 1-5 and reveal the richness of structure and organization of this neuronal population of magnitude similar to that of the spinal Trabalho

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Projections of chemically identified myenteric neurons of the small and large intestine of the mouse

Cited by 93 publications

References 53 publications

Retinoblastoma protein prevents enteric nervous system defects and intestinal pseudo-obstruction

Retinoblastoma protein prevents enteric nervous system defects and intestinal pseudo-obstruction

Building a second brain in the bowel

Number and size of myenteric neurons of the duodenum of adult rats with acute diabetes

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