Kailey Frank, “Examining the Effects of 17β-Estradiol-Induced Gene Expression Following Object Training in the Dorsal Hippocampus of Ovariectomized Female Mice”
Mentor: Karyn Frick, Psychology
Poster #62
17β-estradiol (E2) has long been demonstrated to enhance hippocampus-dependent memory in the dorsal hippocampus (DH) of ovariectomized (OVX) female mice. E2 is known to enhance long-term memory by rapidly activating cell signaling cascades that increase gene transcription in the nucleus. However, the identity and number of the genes regulated by E2 during object memory consolidation remain unclear. As such, the present study aims to provide mechanistic insight into how E2 may selectively enhance gene expression during memory formation. Here, we examined expression of immediate early genes Arc and c-Fos as well as expression of circadian clock gene Per1 in DH tissue collected 1 h following object training in OVX female mice. Adult female mice were OVXed and assigned to either Homecage or Train groups. Mice were first handled 2x/d for 30 s/d for 3 consecutive days. Trained mice were then habituated in an empty box for 5 min/d for 2 consecutive days. During training, mice accumulated 30 s of exploration with two identical objects and were then given an immediate post-training i.p. injection of either vehicle or E2 (0.2 mg/kg) and DH tissue was collected 1 h later for RNAseq analysis of differentially expressed genes. Our preliminary qPCR data indicate that object training increased expression of cFos, Arc and Per1 relative to vehicle-treated homecage controls, suggesting that object training alone drives activity of plasticity-related genes in the DH. Although post-training administration of E2 increased Arc and Per1, but not cFos, expression relative to E2-treated homecage controls, this increase was not significantly different than vehicle-treated trained mice, suggesting E2 does not potentiate training-induced expression of plasticity-related genes. These findings establish a framework for our RNAseq analysis to further identify and characterize expression of learning-induced genes regulated by E2.