ERβ may contribute to the maintaining of radial glia cells polarity through cadherins during corticogenesis.

Laminar organization of neurons in cerebral cortex is essential for normal brain function. Radial glial cells (RGCs), are highly polarized cells that serve as neuronal progenitors and as scaffolds for neuronal migration during construction of the cerebral cortex. Cadherins (E-cadherin and N-cadherin)-based adherins junctions, which anchor apical end-feet of adjacent RGCs to each other at the ventricular surface contribute to sustain the polarity and adhesion of RGCs, therefore affect production of RGCs and radial migration. Estrogen is a steroid hormone and contributes to the organizational sexual differentiation of the brain. We have previously demonstrated that ERβ expression in the cerebral cortex during corticogenesis and contribute to cerebral cortex development. This has been further confirmed by studies from estrogen receptor β knockout (ERβKO) mice, in which lack of ERβ in mice induced abnormal development of cerebral cortical structure, retarded migration of the neurons, and abnormal morphology of RGCs with truncated or less organized radial processes. These indicate that estrogen via ERβ affects RGCs development. Moreover, phenotype analysis in the ERβKO mice has confirmed that estrogen activation ERβ influence the polarity of epithelial tissue and structure integrity by modulating the level of cadherins (E-cadherin and N-cadherin). Thus, we propose that ERβ maybe affect the maintaining the polarity of RGCs through cadherins.