Epidemiology studies indicated that air pollution has been associated with adverse neurological effects in human. Moreover, the secretion of glucocorticoid (GC) affects the mood regulation, and the negative feedback of hippocampal glucocorticoid receptors (GR) inhibits the GC secretion. Meanwhile, the over secretion of GC can interfere the immune system and induce neurotoxicity. In the present study, the human test showed that the secretion of the cortisol in plasma was elevated after exposure in heavy air pollution. In the mouse model, we found that breathing the highly polluted air resulted in the negative responses of the mood-related behavioral tests and morphology of hippocampus, as well as the over secretion of GC in plasma, down regulation of GR, and up-regulation of cytokine and chemokine in the hippocampus. When considering the interrelated trends between the hippocampal GR, inflammatory factors, and plasmatic GC, we speculated that PM_2.5 exposure could lead to the increased secretion of GC in plasma by decreasing the expression of GR in hippocampus, which activated the inflammation response, and finally induced neurotoxicity, suggesting that PM_2.5 exposure negatively affects mood regulation. When combined with the results of the human test, it indicated that exposure to ambient air particles increased the risk of mental disorder.

Cranial neural crest (NC) contributes to the developing vertebrate eye. By multidimensional, quantitative imaging, we traced the origin of the ocular NC cells to two distinct NC populations that differ in the maintenance of sox10 expression, Wnt signalling, origin, route, mode and destination of migration. The first NC population migrates to the proximal and the second NC cell group populates the distal (anterior) part of the eye. By analysing zebrafish pax6a/b compound mutants presenting anterior segment dysgenesis, we demonstrate that Pax6a/b guide the two NC populations to distinct proximodistal locations. We further provide evidence that the lens whose formation is pax6a/b-dependent and lens-derived TGFβ signals contribute to the building of the anterior segment. Taken together, our results reveal multiple roles of Pax6a/b in the control of NC cells during development of the anterior segment. Neural crest (NC) cells are pluripotent embryonic stem cells that originate from neural tissue during early embryogenesis. The origin and fate of NC cells have been studied intensively in various animal species showing that the eye receives input from NC cells. There are several inherited diseases like aniridia, Peters anomaly, Axenfeld-Rieger syndrome and congenital glaucoma affecting structures of the eye derived from NC cells. As of yet, it has remained unclear how the congenital abnormalities of the eye develop in these patients. We have applied genetic tools and multidimensional live imaging to study the dynamics of NC cell behaviour during eye formation. We found that two waves of NC cell populations with different properties contribute to distinct parts of the eye. By using zebrafish mutants as disease models for human anterior segment dysgenesis, we demonstrate that proper guidance of the two NC populations is crucial for a normal development of the anterior segment of the eye.