Vasculature-guided neural migration in mouse cerebellum

Abstract

Neural migration is regarded as a key step for cortical development and cortical lamination. While classical theory holds that immature neurons migrate to their destinations along radial glia, there is some preliminary evidence showing that vasculature is probably involved in that process as well. In this study, we compared vascular development with that of radial glia and the migration of neurons, so that the relationships among them could be elucidated. We found that the radial glial cells and vasculature were highly similar in their distribution and development. For instance, in the external granular layer (EGL, the putative molecular layer), the processes of radial glial cells were arranged in an orderly radial pattern, whereas in the deep areas of the cerebellum, their arrangements were in relative disorder. On the other hand, the vasculatures in EGL were usually orientated radially, which paralleled the projections of radial glia; however, the distribution of vasculature in the internal granular layer (IGL, the putative granular layer) and white matter was in relative disorder as well, similar to the pattern exhibited by radial glial processes. This high harmonization between vasculature and radial glia suggests their interconnected biological relationships during cerebellar development and neural migration. We also observed that a large number of newborn neurons were migrating along blood vessels, suggesting that the vasculature could serve as a scaffold for cell migration. In conclusion, cerebellar vasculature could guide neural migration not only as a platform for biological interaction with radial glia, but also serve scaffolding functions for neural migration.

A Structure‐Activity Relationship between the Veratrum Alkaloids on the Antihypertension and DNA Damage Activity in Mice

“…Neurotoxicity is the one of main Veratru m alkaloid's toxicities . Our previous work demonstrated that veratramine ( 7 ) and 12 β ‐hydroxyveratroylzygadenine ( 9 ) can access to brain tissue through the blood‐brain barrier to cause oxidative stress and consequently lead to DNA damage in mouse cerebellum and cerebral cortex; besides, it also raises the expression of Ogg1 mRNA as a compensatory adjustment to the antioxidant defense status and DNA repair systems . Moreover, jervine ( 8 ), germerine ( 10 ) and neogermbudine ( 11 ) were also confirmed to induce various degrees of oxidative DNA damage in the cerebellum and the cerebral cortex of mice …”