B.A., Psychology, Alma College
M.S., Behavioral Neuroscience, University of Wisconsin-Milwaukee
Ph.D., Behavioral Neuroscience, University of Wisconsin-Milwaukee
University of California, Irvine
Our lab studies the molecular and epigenetic mechanisms that support long-term memory formation, storage, and updating. We want to understand the molecular basis of memory formation and determine how these mechanisms are dysregulated during aging, leading to age-related memory impairments. We use a combination of behavioral techniques, molecular analyses, and in vivo genetic and epigenetic manipulations to understand how memories form in the brain. Specific projects in the lab include:
Circadian clock genes in age-related memory decline
Aging is accompanied by impairments in both long-term memory and circadian rhythmicity. Although it is well-documented that circadian rhythms can influence memory, it is unclear how age-related deficits in these biological processes are related. Our work has shown that a key circadian gene, Period1 (Per1) is repressed by the histone deacetylase HDAC3 in the aging hippocampus, leading to age-related impairments in memory formation. We are currently working to understand how Per1 modulates memory formation in the young and old hippocampus and testing whether other circadian genes may play a similar or complementary role to Per1.
Epigenetic mechanisms underlying fear memory
A second major project in the lab uses fear conditioning and fear extinction to determine the epigenetic and molecular basis of aversive memory. Fear conditioning is a powerful, well-characterized model of memory that allows us to dissect the molecular basis of learning. Using Pavlovian fear conditioning, we aim to understand how epigenetic regulation of Per1 and other circadian genes modulates memory formation in a cell type- and circuit-specific manner. Additionally, we want to understand the mechanisms that support extinction of these aversive associations.
Molecular mechanisms of memory updating
Memory is not permanently stored in a fixed state but, rather, can be modified in response to new, relevant information. Stable memory undergoes a period of vulnerability following a retrieval session, a process termed "reconsolidation," during which the memory may be temporarily prepared to incorporate new information. We have developed a novel memory updating task (termed Objects in Updated Locations (OUL)) that can assess the strength of both the original memory and the updated information in a single test session. In the lab, we aim to understand how memory is modified during updating, using a combination of next-generation sequencing, ensemble-specific cell tagging, and DREADD-mediated manipulations.