Abstract：
:In mice, the compact hippocampal primordium is formed during the prenatal stage by early-generated neurons that migrate from the lateral ventricular zone. However, despite much being understood about the formation of the hippocampus, the molecular mechanisms that maintain the morphology of the hippocampal primordium after its formation remain to be characterized. β-Catenin is a key factor of canonical Wnt signaling and also a component of adherens junctions. Previous embryonic deletion studies have demonstrated that β-catenin is required for early development and generation of granule cells. However, whether β-catenin is involved in the morphological maintenance of the hippocampus as a cell adhesion molecule is still unknown. Here, we report that perinatal deletion of β-catenin in postmitotic neurons and some radial glial cells of hippocampus using CamKIIα-iCre; β-cateninflox/flox conditional knockout mice, leads to disorganization of the radial glial scaffold and consequentially severe defects in hippocampal morphology. We demonstrate that β-catenin is required for maintaining radial glial scaffold possibly via its well-known role in cell adhesion during the perinatal period. These findings provide essential advances into our understanding of the maintenance of the hippocampal primordium during the perinatal period.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Wang HT,Zeng L,Chen Q,Zhang X,Liu JW,Lu TJ,Xiong ZQ,Zheng J,Hu ZLdoi
10.1016/j.neuroscience.2014.08.055subject
Has Abstractpub_date
2015-01-22 00:00:00pages
273-282eissn
0306-4522issn
1873-7544pii
S0306-4522(14)00827-6journal_volume
284pub_type
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