Our research aims to understand the intracellular signaling underlying memory formation and maintenance, and how other factors, including stress, inflammation, and sex can modify these processes and thereby strengthen or weaken memory.
Cytokine Signaling as a Mediator of Fear and Anxiety After Myocardial Infarction.
(Supported by NIH/NIMH K99/R00 MH093459)
After heart attack, major surgery, and other illnesses, patients develop depression and post-traumatic stress disorder. In this project, we aim to understand the mechanisms by which a systemic, inflammatory event (in this case myocardial infarction) causes (1) changes in memory and emotion (2) whether cytokines mediate these alterations in memory; and (3) what intracellular signaling pathways are recruited in this process.
We use a mouse model of myocardial infarction (model of heart attack), together with behavioral tasks, immunostaining (western blot and immunohistochemistry), multiplex analysis, pharmacology and transgenic manipulations to study these questions.
Sex Differences in signaling mechanisms of memory formation
Understanding the intracellular signaling underlying formation of memory is crucial for determining how memory can be altered by environmental events and inflammatory insults. Although a lot is known about the mechanisms in male animals, there is growing evidence that females differ in key receptor and kinase signaling pathways in memory formation. In this project we aim to determine differences in activation and role of intracellular signaling pathways between male and females. This question is particularly important as disorders of memory such as post-traumatic stress disorder are more prevalent in women than men.
We use several Pavlovian conditioning tasks, immunostaining (western blot and immunohistochemistry), multiplex analysis, pharmacology and transgenic manipulations to study these questions.
Memory Reconsolidation
The modification of memory after retrieval has received a growing amount of interest over the past 15 years. The active process that stabilizes memories after retrieval is called “reconsolidation”. Many questions remain about the precise role of this process in the ongoing maintenance of memory. We are interested in the strenghtening of associative memories after retrieval, the molecular mechanisms underlying enhancement of reconsolidation, and the differential roles of new information, emotion, and strengthening of the original memory in this process.
We use Pavlovian conditioning tasks, immunostaining (western blot and immunohistochemistry), multiplex analysis, pharmacology and transgenic manipulations to study these questions.Our research aims to understand the intracellular signaling underlying memory formation and maintenance, and how other factors, including stress, inflammation, and sex can modify these processes and thereby strengthen or weaken memory.