Abstract
The enteric nervous system (ENS) constitutes the largest part of the peripheral nervous system. In recent years, ENS development and its neurogenetic capacity in homeostasis and allostasishave gained increasing attention. Developmentally, the neural precursors of the ENS are mainly derived from vagal and sacral neural crest cell portions. Furthermore, Schwann cell precursors, as well as endodermal pancreatic progenitors, participate in ENS formation. Neural precursors enherite three subpopulations: a bipotent neuron-glia, a neuronal-fated and a glial-fated subpopulation. Typically, enteric neural precursors migrate along the entire bowel to the anal end, chemoattracted by glial cell-derived neurotrophic factor (GDNF) and endothelin 3 (EDN3) molecules. During migration, a fraction undergoes differentiation into neurons and glial cells. Differentiation is regulated by bone morphogenetic proteins (BMP), Hedgehog and Notch signalling. The fully formed adult ENS may react to injury and damage with neurogenesis and gliogenesis. Nevertheless, the origin of differentiating cells is currently under debate. Putative candidates are an embryonic-like enteric neural progenitor population, Schwann cell precursors and transdifferentiating glial cells. These cells can be isolated and propagated in culture as adult ENS progenitors and may be used for cell transplantation therapies for treating enteric aganglionosis in Chagas and Hirschsprung’s diseases.
Highlights
Not all aspects of neuron-glia interaction are fully understood yet, but it is evident that in both systems, physiological neural development and function depend on their functional interaction [18,19]
In the mucosal region of the small intestine of Ret-deficient mice, which do not form an enteric nervous system (ENS), neurons associated with extrinsic nerve fibers were identified [47]. These neurons are derived of Schwann cell precursors (SCP). They develop from trunk neural crest cells (NCC) and undergo neurogenesis independently of the enteric crest-derived cells (ENCC) (Figure 1b)
Repopulation with transplanted ENS progenitors remains challenging unless the microenvironmental conditions can be improved. An example illustrating this problem is the abundance of collagen VI in the tissue environment of postnatal ENCCs in Hirschsprung disease (HSCR) patients with trisomy 21
Summary
Many studies have helped us to understand the molecular mechayears, many studies helped us to understand the molecular mechanism nismInofrecent. In the mucosal region of the small intestine of Ret-deficient mice, which do not form an ENS, neurons associated with extrinsic nerve fibers were identified [47] These neurons are derived of SCPs. These neurons are derived of SCPs They develop from trunk NCCs and undergo neurogenesis independently of the ENCCs (Figure 1b). Specific elimination of the SCPderived neurons resulted in a decrease of the overall enteric neuron numbers in adult mice It seems that ENS formation depends on different sources of neural progenitors to form neurons and glia in the whole gut. It is not known how the diversity of the precursor populations is regulated and how individual cell numbers are balanced. The distribution of neural precursors along the entire bowel, the migration into the specific tissue layers is a highly coordinated process
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