The neural crest‐ and placodes‐derived afferent innervation of the mouse esophagus

Surdenikova, Lenka; Ren, Feng; Nassenstein, Christina; Tatár, M.; Kollárik, Marián

doi:10.1111/nmo.12002

Cited by 31 publications

(46 citation statements)

References 54 publications

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“…No product was amplified from negative (bath) controls ( n = 39) indicating negligible probability of false positive results. In our previous studies we have also reported negligible false positive rates (<1%, n = 640 negative controls) …”

Section: Methodsmentioning

confidence: 59%

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Acid sensitivity of the spinal dorsal root ganglia C‐fiber nociceptors innervating the guinea pig esophagus

Ren

Bánovčin

Kollárik

2015

Neurogastroenterology Motil

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Background Gastroesophageal reflux can cause high acidity in the esophagus and trigger heartburn and pain. However, because of the esophageal mucosal barrier, the acidity at the nerve terminals of pain-mediating C-fibers in esophageal mucosa is predicted to be substantially lower. We hypothesized that the esophageal DRG C-fibers are activated by mild acid (compared to acidic reflux), and express receptors and ion channels highly sensitive to acid. Methods Extracellular single unit recordings of activity originating in esophageal DRG C-fiber nerve terminals were performed in the innervated esophagus preparation ex vivo. Acid was delivered in a manner that bypassed the esophageal mucosal barrier. The expression of mRNA for selected receptors in esophagus-specific DRG neurons was evaluated using single cell RT-PCR. Key Results Mild acid (pH=6.5–5.5) activated esophageal DRG C-fibers in a pH-dependent manner. The response to mild acid at pH=6 was not affected by the TRPV1 selective antagonist iodo-resiniferatoxin. The majority (70–95%) of esophageal DRG C-fiber neurons (TRPV1-positive) expressed mRNA for acid sensing ion channels (ASIC1a, ASIC1b, ASIC2b and/or ASIC3), two-pore-domain (K2P) potassium channel TASK1, and the proton-sensing G-protein coupled receptor OGR1. Other evaluated targets (PKD2L1, TRPV4, TASK3, TALK1, G2A, GPR4 and TDAG8) were expressed rarely. Conclusions & Inferences Guinea pig esophageal DRG C-fibers are activated by mild acid via a TRPV1-independent mechanism, and express mRNA for several receptors and ion channels highly sensitive to acid. The high acid sensitivity of esophageal C-fibers may contribute to heartburn and pain in conditions of reduced mucosal barrier function.

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Section: Methodsmentioning

confidence: 59%

“…Spinal T2 and T3 DRG ganglia were harvested 10–15 days after the injections. Single cell RT‐PCR was performed on individual neurons as described previously . The sensory ganglia were dissected, enzymatically dissociated, and the neurons were plated on poly‐ d ‐lysine/laminin‐coated coverslips.…”

Section: Methodsmentioning

confidence: 99%

Acid sensitivity of the spinal dorsal root ganglia C‐fiber nociceptors innervating the guinea pig esophagus

Ren

Bánovčin

Kollárik

2015

Neurogastroenterology Motil

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“…As germline Cdh1 knockout led to embryonic lethality [8], we crossed Wnt1-Cre mice [22] Figure S2A). We harvested RNAs from different tissues and found reduced Cdh1 mRNA levels in dorsal root ganglion of Cdh1 Wnt1 mice (Supplementary information, Figure S2B) [23]. Intriguingly, we found that Cdh1…”

Section: Cdh1 Conditional Knockout Mice Displayed Various Craniofaciamentioning

confidence: 75%

Cdh1 regulates craniofacial development via APC-dependent ubiquitination and activation of Goosecoid

et al. 2016

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Craniofacial anomalies (CFAs) characterized by birth defects of skull and facial bones are the most frequent congenital disease. Genomic analysis has identified multiple genes responsible for CFAs; however, the underlying genetic mechanisms for the majority of CFAs remain largely unclear. Our previous study revealed that the Wwp2 E3 ubiquitin ligase facilitates craniofacial development in part through inducing monoubiquitination and activation of the paired-like homeobox transcription factor, Goosecoid (Gsc). Here we report that Gsc is also ubiquitinated and activated by the APC Cdh1 E3 ubiquitin ligase, leading to transcriptional activation of various Gsc target genes crucial for craniofacial development. Consistenly, neural crest-specific Cdh1-knockout mice display similar bone malformation as Wwp2-deficient mice in the craniofacial region, characterized by a domed skull, a short snout and a twisted nasal bone. Mechanistically, like Wwp2-deficient mice, mice with Cdh1 deficiency in neural crest cells exhibit reduced Gsc/ Sox6 transcriptional activities. Simultaneous deletion of Cdh1 and Wwp2 results in a more severe craniofacial defect compared with single gene deletion, suggesting a synergistic augmentation of Gsc activity by these two E3 ubiquitin ligases. Hence, our study reveals a novel role for Cdh1 in craniofacial development through promoting APC-dependent non-proteolytic ubiquitination and activation of Gsc.

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“…Its main function is to transport the food into the stomach by a propulsive contraction wave. Peristaltic movement of the esophagus is controlled by nerves of vagal motor neurons and the ganglionated myenteric plexus . The myenteric plexus of the esophagus (a part of the enteric nerve system) is derived from the neural crest, while the vagal neurons are derived from both the neural crest and cranial placodes .…”

Section: Introductionmentioning

confidence: 99%

“…Peristaltic movement of the esophagus is controlled by nerves of vagal motor neurons and the ganglionated myenteric plexus . The myenteric plexus of the esophagus (a part of the enteric nerve system) is derived from the neural crest, while the vagal neurons are derived from both the neural crest and cranial placodes . Esophageal innervation is first observed in the rostro‐most regions of the esophagus at E13, and develops in a rostrocaudal progression that is coincident with esophageal muscle differentiation .…”

Section: Introductionmentioning

confidence: 99%

Loss of JAM-C leads to impaired esophageal innervations and megaesophagus in mice

Zhang

et al. 2015

Dis Esophagus

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Megaesophagus is a disease where peristalsis fails to occur properly and esophagus is enlarged. The etiology and mechanism of megaesophagus are not well understood. In this study, we reported that junctional adhesion molecule C (JAM-C) knockout mice on a C57/B6 background developed progressive megaesophagus from embryonic day (E) 15.5 onward with complete penetrance. JAM-C knockout mice exhibited a significant reduction in the number of nerve fibers/ganglia in the wall of the esophagus. However, histological analysis revealed that the esophageal wall thickness and structure of JAM-C knockout mice at embryonic stages and young adult were comparable to that of control littermates. Thus, megaesophagus observed in JAM-C knockout mice could be attributed, at least in part, to impaired esophageal innervations. Our data suggest JAM-C as a potential candidate gene for human megaesophagus, and JAM-C knockout mice might serve as a model for the study of human megaesophagus.

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The neural crest‐ and placodes‐derived afferent innervation of the mouse esophagus

Cited by 31 publications

References 54 publications

Acid sensitivity of the spinal dorsal root ganglia C‐fiber nociceptors innervating the guinea pig esophagus

Acid sensitivity of the spinal dorsal root ganglia C‐fiber nociceptors innervating the guinea pig esophagus

Cdh1 regulates craniofacial development via APC-dependent ubiquitination and activation of Goosecoid

Loss of JAM-C leads to impaired esophageal innervations and megaesophagus in mice

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