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Abstract
S100B is expressed in various types of glial cells and is involved in regulating many aspects of their function. However, little is known about its role during nervous system development. In this study, we investigated the effect of inhibiting the onset of S100B synthesis in the development of the enteric nervous system, a network of neurons and glia located in the wall of the gut that is vital for control of gastrointestinal function. Intact gut explants were taken from embryonic day (E)13.5 mice, the day before the first immunohistochemical detection of S100B, and cultured in the presence of arundic acid, an inhibitor of S100B synthesis, for 48 h. The effects on Sox10-immunoreactive enteric neural crest progenitors and Hu-immunoreactive enteric neurons were then analyzed. Culture in arundic acid reduced the proportion of Sox10+ cells and decreased cell proliferation. There was no change in the density of Hu+ enteric neurons, however, a small population of cells exhibited atypical co-expression of both Sox10 and Hu, which was not observed in control cultures. Addition of exogenous S100B to the cultures did not change Sox10+ cell numbers. Overall, our data suggest that cell-intrinsic intracellular S100B is important for maintaining Sox10 and proliferation of the developing enteric glial lineage.
Highlights
The enteric nervous system (ENS) is a large, complex division of the autonomic nervous system
In order to investigate the role of enteric glia in ENS development, we first characterized the proportion of enteric neural crest-derived cells (ENCCs) expressing the glial marker, S100B, at various embryonic and early postnatal ages
Using Wnt1-Cre;R26R-GCaMP3 mice, where all ENCCs express the reporter protein, GCaMP3, which can be detected using anti-GFP antisera, we examined the proportion of S100B+/GFP+ cells of the myenteric plexus in the duodenum and colon at E13.5, E14.5, E16.5 and P0 mice
Summary
The enteric nervous system (ENS) is a large, complex division of the autonomic nervous system. All the neurons and glia of the ENS arise from neural crest cells that migrate into the gut during development (Yntema and Hammond, 1954; Le Douarin and Teillet, 1973). Another marker of enteric glia in the mature ENS is initially found in all undifferentiated ENCCs (Young et al, 2002, 2003). It is downregulated in enteric neurons, but maintained in glial precursors and the majority of mature enteric glia (Young et al, 2003; Laranjeira et al, 2011; Boesmans et al, 2015b). Sox expression is important for peripheral glia development (Britsch et al, 2001) and recently has been found to promote the expression of S100B in Schwann cell precursors to induce their differentiation (Fujiwara et al, 2014)
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