Neurofilament formation and synaptic activity are delayed in the myenteric neurons of the rat fetus with gastroschisis

Vannucchi, Maria Giuliana; Midrio, Paola; Zardo, Claudio; Faussone–Pellegrini, Maria Simonetta

doi:10.1016/j.neulet.2004.03.095

Cited by 19 publications

(20 citation statements)

References 16 publications

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“…3 ), the longer the myenteric plexus will remain immature. These are additional results to those found by Vannucchi et al [10,12] which were presented for only 1 gestational day, E18.5. Preterm delivery could help to avoid some complications after birth and could improve the postoperative period, be less costly, and shorten the requirements for total parenteral nutritional [29] .…”

Section: Discussionsupporting

confidence: 86%

“…By means of ␣ -internexin immunoreactivity in gastroschisis bowel loops in E18.5 [12] found that there was diminished reaction and consequent delay in neuronal maturation in addition to disorganization of the myenteric plexus. Both findings could explain the alterations in synaptic activity of the myenteric neurons that affect the control of intestinal motility in gastroschisis.…”

Section: Discussionmentioning

confidence: 95%

“…These characteristics may function as markers of the degree of bowel lesion expression and may be measured by the presence of neurofilaments along the intrinsic intestinal nervous plexus [11,12] . Recently other authors have reported that the interstitial cells of Cajal serve as electrical pacemakers, providing pathways for the active propagation of slow waves, acting as mediators of enteric motor neurotransmission, and playing a role in afferent neural signaling; they also discuss the complexity of the physiology and histological identification of the interstitial cells of Cajal [13] .…”

Section: Introductionmentioning

confidence: 99%

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Maturity of the Myenteric Plexus Is Decreased in the Gastroschisis Rat Model

França¹,

Langone²,

Hoz³

et al. 2007

Fetal Diagn Ther

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Background: Amniotic fluid (AF) and its components, such as fetal urine and meconium, may lead to intestinal alterations in gastroschisis, which cause immaturity of the myenteric plexus and consequent intestinal hypomotility and malabsorption. In this study we identified morphological and histological alterations of the intestine and the myenteric plexus with two different times of exposure to AF. Methods: The experimental gastroschisis was achieved at two different gestational ages, on day 18.5 (E18.5) and day 19.5 (E19.5) of gestation, in fetal rats which were divided into 3 subgroups: control, sham and gastroschisis. We measured fetal body weight (BW), intestinal weight (IW) and intestinal length (IL). The layers of intestinal wall and myenteric plexus were evaluated by hematoxylin and eosin staining (HE staining) and immunofluorescence (α-internexin), respectively. Results: BW was not significantly different among the control, sham and gastroschisis groups at both ages. IW and IL were larger and shorter, respectively, in the gastroschisis fetuses (p < 0.001) at both ages. Intestinal diameters and wall layers presented significant differences among control, sham and gastroschisis fetuses at both ages (p < 0.001), but the time of exposure to AF compromised the serous membrane, D-II (diameter II, p < 0.001) and IL (p = 0.001). α-Internexin presented more intensive immunoreactivity in gastroschisis fetuses at E18.5. Conclusions: In gastroschisis, the longer the time of exposure to AF, the more severe bowel impairment will be, especially with regard to IL and the serous layer, and the more immature the myenteric plexus will be.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Maturity of the Myenteric Plexus Is Decreased in the Gastroschisis Rat Model

França¹,

Langone²,

Hoz³

et al. 2007

Fetal Diagn Ther

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“…Whether the observed abnormal development of the ENS might be, at least in part, caused by exposure to the AF is currently unknown. However, previous data obtained from surgical created GS models in which the artificial exposure of the fetal bowel also demonstrated a significant disturbance of ENS organization and maturation (27,28). Future studies however are required to reveal the specific cellular mechanisms that are accountable for the observed morphologic changes of the ENS in the EI.…”

Section: Discussionmentioning

confidence: 96%

Gastroschisis in Mice Lacking Aortic Carboxypeptidase-Like Protein Is Associated With a Defect in Neuromuscular Development of the Eviscerated Intestine

et al. 2010

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Mice lacking aortic carboxypeptidase-like protein (ACLP) exhibit a gastroschisis (GS) like abdominal wall defect. The objectives of this study were to evaluate the pathophysiological features of GS in ACLP Ϫ/Ϫ mice and to characterize the neuromuscular development of the eviscerated intestine (EI). ACLP Ϫ/Ϫ mice were created by heterozygous mating from previously generated mice with targeted disruption of ACLP. Specimens were processed for H&E, and immunohistochemistry for smooth muscle cells [SMC, ␣-smooth muscle actin (␣-SMA) antibody], interstitial cells of Cajal (ICC, c-kit-antibody), neural crest cells (NCC, Hox-b5-antibody), and enteric neurons (EN, PGP9.5-, ␣-internexin, and synaptophysin antibody). From 47 fetuses genotyped, 13 (27.7%) were wild type, 20 (42.5%) were heterozygous, and 14 (29.8%) were ACLP homozygous. In GS mice, expression of c-kit, Hox-b5, PGP-9.5, ␣-internexin, and synaptophysin were almost completely absent and only faint ␣-SMA expression was seen in the EI. In contrast, c-kit, Hox-b5, PGP9.5, ␣-internexin, synaptophysin, and ␣-SMA expression in intra-abdominal intestine in GS fetuses was the same as control intestine. The defect observed in ACLP Ϫ/Ϫ mice closely resembles GS. Absence of ICC, NCC, EN, and immature differentiation of SMC supports an associated defect in neuromuscular development that is restricted to the EI. (Pediatr Res 68: 23-28, 2010)

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“…Intestinal neurofilament formation also appeared immature, demonstrating delayed cytoskeletal organization and reduced synaptic activity in the myenteric neurons in the rat model of GS [174]. Immunohistochemical analysis of GS intestine showed delayed differentiation of smooth muscle cells and interstitial cells of Cajal, with the most severely affected bowel loops demonstrating the most significant aberration in pacemaker cell morphology [175].…”

Section: Surgically Created Gastroschisis Modelsmentioning

confidence: 99%