Abstract
Abstract Breast carcinoma amplified sequence 2(BCAS2) is involved in Prp19/CDC5 Lspliceosome complex for regulation of RNA splicing. Exon array analysis indicated that β-catenin was one of BCAS2-targeted gene. Disruption of Wnt/β-catenin signaling is involved in several neurodegenerative diseases such as Alzheimer’s disease (AD). Current report of other group demonstrated that the RNA expression of BCAS2 is reduced in the microarray analysis of AD patients. Recently, we used the Cre/loxP system driven by CaMKIIα to generate BCAS2 conditional knock out (cKO) in postnatal forebrain, which causes microcephaly-like, dendritic malformation, poor learning and memory phenotypes partly reasons from down-regulation of β-catenin. In this study, the reactive gliosis in cKO mice was extensively measured and compared with WT mice. The selective microgliosis was found in the cornu ammonis1 stratumradiatum (CA1 Rad) and dentate gyrus molecular layer (DG Mo) but did not exhibit astrogliosis in cKO compared with WT mice, which confirmed depletion of BCAS2 in the forebrain caused neural defect. Lithium, an inhibitor of glycogen synthase kinase-3β (GSK-3β). Lithium treatment to cKO mice could improve their spatial learning and memory capability using passive avoidance and Morris water maze; and reduced selective microgliosis in the molecular layer (DG Mo)compared with untreated cKO mice. Taken together, BCAS2 may be a neuron protective factor to inhibit microgliosis.
Published Version
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