Validation experiment designed to validate causal mechanisms targeting Nr3c1 in pregnant mice and offspring. Primary outcome: differential gene expression in hippocampus
This study investigated the molecular biological changes in fetal hippocampus following prenatal exposure to haloperidol (HAL) as a model of schizophrenia-like developmental disruption. Pregnant mice were administered haloperidol (1 mg/kg/day) during gestation, and the hippocampal tissue from offspring was analyzed using RNA-sequencing to identify differentially expressed genes. The study aimed to understand how prenatal antipsychotic exposure, an environmental risk factor, induces apoptotic neurodegeneration and cognitive impairment similar to schizophrenia. RNA-sequencing revealed significant gene expression changes, with particular focus on Nr3c1 mRNA upregulation. The research also included in silico analysis to predict microRNA regulation of the observed gene expression changes, specifically investigating miR-137-3p as a potential regulator of Nr3c1 expression.
Pregnant mice administered HAL (1 mg/kg/day), offspring hippocampus harvested for RNA-sequencing analysis, qPCR validation of selected genes, in silico prediction of miRNA regulation
Altered gene expression patterns in hippocampus of HAL-exposed offspring, particularly changes in Nr3c1 expression and miR-137-3p regulation
Significant differential gene expression (P < 0.05 and q < 0.05), successful qPCR validation of RNA-seq findings
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