Current Projects
Our lab uses a combination of behavioral and neurobiological techniques to understand how memories are formed and retrieved in the brain. We measure behavioral performance both during and following associative learning in which animals learn to associate a neutral stimulus, like a white noise or physical environmental chamber (i.e., context) with a brief footshock. We examine how neural manipulations, using both optogenetic and pharmacological techniques, affect memory acquisition, consolidation, and its subsequent retrieval. We then examine molecular markers associated with these processes using immunofluorescence and microscopy.
The role of the retrosplenial cortex in memory formation and retention.
The retrosplenial cortex makes critical contributions to learning and memory, particularly in situations in which the information acquired is complex. We use a variety of behavioral measures, including trace and contextual fear conditioning and passive avoidance learning, in combination with an optogenetic approach to determine a causal, time-dependent role for the retrosplenial cortex in learning and memory. We are particularly interested in determining how distinct subregions along the anterior-posterior axis of the retrosplenial cortex differ in their contributions to associative learning and memory.
Sagittal view of the rodent brain with the retrosplenial cortex highlighted in green.
Relevant Publications:
Trask, S., Pullins, S.E., Ferrara, N.C., & Helmstetter, F.J. (2021). The anterior retrosplenial cortex encodes event-related information and the posterior retrosplenial cortex encodes context-related information during memory formation. Neuropsychopharmacology, 43, 1386-1392. https://doi.org/10.1038/s41386-021-00959-x
Trask, S., Ferrara, N.C., Jasnow, A.M., Kwapis, J.L. (2021). Contributions of the cingulate-retrosplenial cortical axis to associative learning and memory: A proposed circuit for persistent memory maintenance. Neuroscience & Biobehavioral Reviews, 130, 178-184. https://doi.org/10.1016/j.neubiorev.2021.08.023
Trask, S., Ferrara, N. C., Grisales, K., & Helmstetter, F. J. (2021). Optogenetic inhibition of either the anterior or posterior retrosplenial cortex disrupts retrieval of a trace, but not delay, fear memory. Neurobiology of Learning and Memory, 185, 107530. https://doi.org/10.1016/j.nlm.2021.107530
Trask, S., & Helmstetter, F.J. (2022). Unique roles for the anterior and posterior retrosplenial cortices in encoding and retrieval of memory for context. Cerebral Cortex, in press. https://doi.org/10.1093/cercor/bhab436
Age-related neural degeneration and its effects on memory.
Aging is associated with zif268 protein accumulation and reductions in proteasome activity (measured using Rpt6 phosphorylation) in both the medial prefrontal cortex (top) and the retrosplenial cortex (bottom).
Normal aging is accompanied by decreases in the ability to accurately form and recall episodic memories. In rats, this is likely attributable to degeneration of a large neural circuit needed to support memory in aged animals, including the retrosplenial and medial prefrontal cortices. We are interested in characterizing these memory deficits in a wide array of behavioral assays, as well as using immunofluorescence and proteasome assays to understand the changes associated with poorer memory performance in aged animals. We aim to use this understanding to facilitate memory formation using a variety of approaches to target specific patterns of degeneration.
Relevant Publications:
Trask, S., Dulka, B. N., & Helmstetter, F. J. (2020). Age-related memory impairment is associated with increased zif268 protein accumulation and decreased Rpt6 phosphorylation. International Journal of Molecular Sciences, 21, 5352. https://doi.org/10.3390/ijms21155352
Dulka, B. N., Trask, S., & Helmstetter, F. J. (2021). Age-related memory impairment and sex-specific alterations in phosphorylation of the Rpt6 proteasome subunit and polyubiquitination in the basolateral amygdala and medial prefrontal cortex. Frontiers in Aging Neuroscience, 13, 163. https://doi.org/10.3389/fnagi.2021.656944
Trask, S., & Fournier, D. I. (2022). Examining a role for the retrosplenial cortex in age-related memory impairment. Neurobiology of Learning and Memory, 189, 107601 https://doi.org/10.1016/j.nlm.2022.107601
Lab News
March, 2023: Payton Robinson earns a Ross Fellowship, selected on the basis of academic excellence, to fund her PhD work in the Department of Psychological Sciences.
March, 2023: Undergraduate research assistant, Destine Williams, earns a fellowship to fund her summer research in the Trask Lab through the Summer Research Opportunity Program.
January, 2023: Sydney receives a collaborative research grant from the Research Corporation for Science Advancement and the Frederick Gardner Cottrell Foundation to study how early-life adversity impacts biological and cognitive aging.
January, 2023: Lab members, Ellie Bonanno, Erisa Met Hoxha, and Payton Robinson, earn coauthorship on a research article, "Fear reduced through unconditional stimulus deflation is behaviorally distinct from extinction and differentially engages the amygdala."
December, 2022: Undergraduate research assistant, Michael Kuczajda, earns coauthor ship on a review, "The lifetime impact of stress on fear regulation and cortical function."
July, 2022: The lab, in collaboration with the Brashier Lab, receives a research grant from the Purdue HHS Healthy Lifestyles and Vital Longevity signature area to study the neural and molecular correlates of cognitive decline in aging humans and rodents.
July, 2022: Sydney is chosen as a Scialog Fellow for the Molecular Basis of Cognition. More information on the program is available here.
June, 2022: The lab is featured on Purdue's 'Lab Culture' Series.
May, 2022: Graduate student, Erisa Met-Hoxha, earns a BRIDGE summer fellowship from the College of Health and Human Sciences.
April, 2022: The lab receives a research grant from PIIN and CEREBBRAL to study how upregulation of proteasome activity in the retrosplenial cortex impacts age-related cognitive decline.