Project description:The Ts1Cje mouse model of Down syndrome (DS) has partial triplication of mouse chromosome 16 (MMU16), which is partially homologous to human chromosome 21. The mouse model develops various neuropathological features identified in DS individuals. We analysed the effect of partial triplication of the MMU16 segment on global gene expression in the cerebral cortex, cerebellum and hippocampus of Ts1Cje mice at 4 time-points; postnatal day (P)1, P15, P30 and P84. RNA was extracted from thre brain regions (Cerebral cortex, hippocampus and cerebellum) for hybridization to arrays from 3 pairs of Ts1Cje and disomic C57BL/6 littermate control for each timepoints at postnatal (P) day 1, P15, P30 and P84.
Project description:The developing brain is particularly sensitive to ethanol during the brain growth spurt or synaptogenesis (third human trimester equivalent). This has been shown to lead to abnormal brain development and behavioural changes in the adult mouse that are relevant to those seen in humans with fetal alcohol spectrum disorders (FASD). We evaluated the long-term (postnatal day 60 young adult) gene expression changes that occur in the brain due to ethanol exposure during synaptogenesis. We used microarray analyses to evaluate the changes in brain gene expression at postnatal day 60 that occur due to ethanol treatment at postnatal days 4 and 7 (synaptogenesis). To generate samples, C57BL/6J pups were injected with ethanol (experimental) or saline (control) at postnatal days 4 and 7. Pups were weaned at postnatal day 25 and sacrificed at postnatal day 60. Total RNA was extracted from whole brain tissue and RNA from three male mice from three different litters were pooled as one biological replicate. Each male ethanol-treated mouse represented in a sample was matched by a control littermate present in a control sample. This study consists of two biological replicates for each experimental group (total mice used was n=12).
Project description:In this study, gene expression of brain from postnatal (day 5) and aging (week 70) mice (C57BL/6J) was profiled. The data was used to infer transcriptional network of genes associated with epigenetic clock and GnRHR pathway in the brain. The results of this study suggested that brain aging originated early-in life.
Project description:Gene expression profiling in C57BL/6J and A/J mouse inbred strains reveals gene networks specific for brain regions independent of genetic background Comparison of whole genome expression data of amygdala and hippocampus of both C57BL/6J and A/J mouse inbred strains using a network approach
Project description:The developing brain is particularly sensitive to ethanol during the brain growth spurt or synaptogenesis (third human trimester equivalent). This has been shown to lead to abnormal brain development and behavioural changes in the adult mouse that are relevant to those seen in humans with fetal alcohol spectrum disorders (FASD). We evaluated the acute (4h post-treatment) gene expression changes that occur in the brain due to ethanol exposure during synaptogenesis (postnatal day 7). We used microarray analyses to evaluate the changes in brain gene expression at postnatal day 7 that occur due to ethanol treatment at postnatal day 7 (synaptogenesis). To generate samples, C57BL/6J pups were injected with ethanol (experimental) or saline (control) at postnatal day 7 (2 x 2.5 g/kg at 0h and 2h). Pups were sacrificed 4 hours following the initial injection. Total RNA was extracted from whole brain tissue and RNA from three male mice from three different litters were pooled as one biological replicate. Each male ethanol-treated mouse represented in a sample was matched by a control littermate present in a control sample. This study consists of two experimental (ethanol-treated) biological replicates and four control (saline vehicle-treated) replicates (total mice used was n=18).
Project description:Since normal brain function depends upon continuous oxygen delivery and short periods of hypoxia can precondition against subsequent ischemia, this study examined the effects of brief hypoxia on the whole genome transcriptional response in adult mouse brain. Genomic expression profiling was perfromed for individual brain regions of the adult mice following the entire time course of hypoxia preconditioning. Adult C57BL/6 male mice were exposed to systemic preconditioning hypoxia (8% O2 ) for 3 hr and allowed to recover in normoxia for 24 hr. The mouse brains were removed and dissected into individual brain regions at multiple time points during the 3hr hypoxia and subsequent 24hr reoxygenation periods. Total RNA was purified from the human whole blood or individual mouse brain regions. Genomic scale gene expression was then measured with Affymetrix Mouse Expression 430 2.0 arrays.