Enteric nervous system can regenerate in zebrafish larva via migration into the ablated area and proliferation of neural crest-derived cells

Enteric nervous system (ENS) which is derived from neural crest is essential for gut function and its deficiency causes severe congenital diseases. Since capacity of ENS regeneration in mammals is limited, additional complimentary models would be useful. Here, we show that the ENS in zebrafish larva at 10-15 days post-fertilization is highly regenerative. The number of enteric neurons (ENs) recovered to ∼50% of the control by 10 days post-ablation (dpa) after their laser ablation. Using transgenic lines in which enteric neural crest-derived cells (ENCDCs) and ENs are labeled with fluorescent proteins, we live-imaged the regeneration process, and found covering by neurites extended from the unablated area and entry of ENCDCs in the ablated areas by 1-3 dpa. BrdU assay suggested that ∼80% of the ENs and ∼90% of the Sox10-positive ENCDCs therein at 7dpa are generated through proliferation. Thus the ENS regeneration involves proliferation, entrance and neurogenesis of ENCDCs. This is the first report regarding the regeneration process of the zebrafish ENS; our findings provide a basis for further in vivo research at single-cell resolution in the vertebrate.

Biomass Cellulose Nanoparticles Display Considerable Neurotoxicity in Zebrafish

BackgroundThe widespread use of nanomaterials poses a great threat to human living environments. Among them, biomass cellulose nanoparticle (CN) is one of the widely used nanomaterials. To date, the toxicity of CNs during embryonic development remains undetermined. In this study, we exposed zebrafish embryos to cellulose nanofibrils (CNFs) and cellulose nanocrystals (CNCs) to evaluate the toxicity of these CNs. ResultsExposure to CNFs or CNCs below 30 mg/ml exhibited no dose-dependent increases in malformation and mortality in zebrafish embryos. Then we demonstrated that CNs were highly enriched in zebrafish embryo via imaging analysis of embryos treated with FITC-coupled CNCs. In addition, we found that CNF or CNC exposure resulted in compromised motor ability of zebrafish larva. Furthermore, it was revealed that the differentiation and the morphogenesis of motor neurons were significantly interrupted. While, blood vessels were normally patterned, suggesting the specific neurotoxicity of those materials. Transcriptome sequencing assay demonstrated that the neurotoxicity of CNs in the motor neurons might be attributed to the expression alteration of neural genes. ConclusionWe found that the specific neurotoxicity of CNF and CNC using zebrafish model. CNF or CNC exposure interrupted the morphogenesis of motor neurons, which resulted in the compromised motor ability of zebrafish larva. In addition, the neurotoxicity of CNs in the motor neurons might be attributed to the expression alteration of neural genes.