Presenters: Austin Stewart, College of Family, Home, and Social Sciences, Neuroscience
Authors: Austin Stewart, Matthew Holdaway
Faculty Advisor: Jeffrey Edwards, College of Life Sciences, Physiology and Developmental Biology
Institution: Brigham Young University
Synaptic plasticity is the cellular mechanism that allows the brain to change and learn in response to environmental stimulus or the lack thereof. In the hippocampus, an area known to be important for memory formation and consolidation, long-term potentiation (LTP) is a critical mechanism for memory formation; LTP contributes to the strengthening of synapses (connections between communicating neurons). An opposing process that contributes to our ability to “forget” or hone particular memory formation by weakening synaptic strength is known as long-term depression (LTD). Both LTP and LTD are critical in forming, strengthening, and honing neuronal connections in the hippocampus to facilitate learning. While there is significant research on LTD, it has been general and there are many contradicting opinions about the various pathways involved. Additionally, there is little research on LTD as a reversal mechanism of LTP—a process in which something that was once potentiated (LTP—a strengthened synapse) is put under LTD conditions to weaken the synapse; this is commonly referred to as depotentiation (DP). In our study, we explore DP and attempt to address these disputes. We will focus on two major receptors found in hippocampal memory pathways: N-methyl-D-aspartate receptors (NMDARs—ion-based receptors found in the postsynaptic membrane) and metabotropic glutamate receptors (mGluRs—second messenger system-based receptor involved in producing longer lasting effects of LTP/LTD). Using neuropharmacology and electrophysiology, we will activate and/or block these various receptors to determine which pathways are essential to DP. To resolve the inconsistencies in previous research, we will also consider how the age of mice and the duration of LTP affect the pathways found in DP circuitry. Our hope is that by expanding our knowledge of DP as a “forgetting” mechanism, it will influence research on the underlying causes of neurological memory disorders.