Grant: Master's Award: Canada Graduate Scholarships

The steroid hormone 17ß-estradiol (E2), often referred to as simply estrogen, has profound effects on synaptic plasticity in both males and females. Synaptic plasticity refers to structural and functional changes that occur in the brain, necessary for many of the fundamental processes of learning and memory. The synthesis of E2 occurs independently of the gonads in a variety of brain regions including the hippocampus. The two estrogen receptors, ERa and ERß, are expressed in the hippocampus, yet synaptic plasticity is most tightly associated to the activation of ERß. As a neuromodulator, E2 can induce macroscopic changes to dendritic branching and spine formation, and initiate the activation of numerous signaling cascades involved in synaptic plasticity. In female animals, the stage of the estrous cycle can significantly influence the outcome of experiments examining biological models of learning and memory. For this reason the majority of research into synaptic plasticity has come from animal models focusing almost entirely on males. Therefore, examining differences in synaptic plasticity in both males and females in important in fully understanding the neuronal basis of learning and memory. Unfortunately there is little basic research on how of E2 exposure affect the N-methyl D-aspartate receptor (NMDARs), the central nervous system exctitatory receptor most closely associated with learning and memory. NMDARs are subject to a wide variety of modifications that regulate its function. This research aims to address the nuromodulatory role of E2 on the NMDAR, and how specific activation of either ERa or ERß receptor can affect NMDAR function in the hippocampus.