My research interests are memory and learning. I am interested, specifically, in trauma induced memory related dysfunctions and the underlying mechanisms that cause them. My current research is aimed at elucidating some of these processes. My project uses Activity-regulated cytoskeletal protein (Arc), a marker for synaptic plasticity, to determine the effects of a stressful event on the learning processes in the anterior cingulate cortex (ACC). Malin and McGaugh (2006) showed that their ACC is involved in the aversive, one trial Inhibitory avoidance (IA) task, in particular the rACC is involved in processing the shock aspect of the task. In humans, the ACC is known for its involvement in processing the emotional saliency of pain, and appears to be hyperactive in PTSD subjects. Understanding the processes which occur in this area after a stressful event is therefore important to understanding the underlying neural dysfunctions in PTSD.
My research, so far, has shown that Arc protein expression in their ACC is important for the long-term consolidation of memory for IA training, up to six hours after training. This is in opposition to most consolidation data, suggesting that consolidation of a memory occurs within a few hours after training.
I have also shown that the basolateral complex of the amygdala (BLA) is modulating the expression of Arc and a similar immediate early gene CaMKIIα in the rACC after training on an IA task. This is similar to work shown by McIntyre and colleagues (2005) showing that the BLA is modulating Arc protein expression in the hippocampus.
Similarly, I have shown, in conjunction with Jayme McReynolds in the lab, that the stress hormone corticosterone works with the BLA to increase Arc protein in the rACC. Systemic injections of corticosterone, when paired with IA training, increase Arc protein in the rACC. This effect is dependent on β-noradrenergic activity in the BLA.
I am interested in examining the mechanisms that underlie long-term memory formation, especially long-term memory for emotional events. The stress hormones corticosterone and epinephrine produce responses in the basolateral complex of the amygdala (BLA), which in turn influences long-term memory by modulating plasticity in other areas of the brain. I use a behavioral learning and memory tasks as well as pharmacological manipulations of the BLA in order to investigate how emotionally arousing memories are formed. Because I am interested in the BLA influence on the other memory-related brain regions, I examine post-training expression of plasticity-related proteins in the relevant structures using western blotting and immunohistochemistry.
We are currently testing the effect of vagus nerve stimulation (VNS) on exposure therapy using a rodent model. Exposure therapy is a primary tool used in the treatment of posttraumatic stress disorder (PTSD), phobia, obsessive compulsive disorder, and addiction. Because the vagus nerve is uniquely positioned to modulate both memory storage and anxiety, we are attempting to use VNS as an adjunct to exposure therapy with the aim of facilitating the extinction of maladaptive memories. If VNS is effective in facilitating exposure therapy effects, it may prove to be a useful approach in the treatment of patients with anxiety disorders.