I earned a BS in Biology & Psychology from the University of Massachusetts and a MS in Biology from Fordham University. My past work explored how trait anxiety and environmental conditions create vulnerabilities to drug addiction. I have also studied White Nose Syndrome – an emerging fungal disease in bats. Currently, I am interested in understanding the neural circuitry underlying sex differences in psychiatric disorders. As a PhD student in Dr. Burghardt’s lab, I am investigating the effect of serotonin on fear learning circuitry in male and female mice. I also enjoy working on jigsaw puzzles.

Project

There is considerable evidence that an acute increase in serotonin as caused by selective serotonin reuptake inhibitor (SSRI) treatment can lead to increased anxiety and depressive symptoms. However, the neural circuitry underlying these effects is not established. Recent animal work indicates the bed nucleus of the stria terminalis (BNST) may mediate these effects. To better elucidate serotonin’s action in this region, I optogenetically activate serotonin while animals undergo fear learning. Preliminary data reveals that elevated serotonin levels in the BNST enhance fear response in female, but not male, mice. To understand how this modulates other regions important for fear learning, I am conducting awake-behaving electrophysiological recordings in several brain regions. During fear learning, local field potentials from the BNST and the central nucleus of the amygdala—an important output nuclei in fear learning—are recorded to determine alterations in neuronal activity.

In the late 1980s, the first selective serotonin reuptake inhibitor (SSRI), Prozac, was introduced as a new treatment for depression. Today, SSRIs are among the most commonly prescribed psychiatric drugs in the United States. SSRIs elevate serotonin levels in the brain upon administration, but there is a significant delay in relief of symptoms (6-8 weeks) despite the immediate increase in serotonin availability. Furthermore, initial SSRI treatment is often associated with an increase in negative emotions such as depression, anxiety, and even suicidal ideation. This paradox in SSRI treatment is not well understood. 

Although typically thought of as the “happy” neurotransmitter in popular culture, in actuality serotonin contributes to a myriad of moods, behaviors, and brain processes. The amplified anxiety or depression accompanying the elevation of serotonin during initial SSRI treatment, directly contradicts the “happy” narrative. Serotonin projections are located throughout the entire brain making isolating the regions contributing to these negative emotions difficult. To get around this problem I spent the summer utilizing a technique called optogenetics: using a genetically modified mouse strain, I can control serotonin release in an awake-behaving mouse via a surgically implanted fiber optic. Hooking up an animal to the laser system allows me to stimulate serotonin release in discrete brain regions, something you are not able to achieve with pharmacological methods.

My mentor, Dr. Nesha Burghardt, previously found that acute SSRI administration enhances fear learning (a protocol used to study negative emotional memories) in an animal model. This mirrors the findings seen in clinical human research. Her initial results also pointed to a brain region known as the bed nucleus of the stria terminalis (BNST) as possibly mediating these effects. The BNST is a complicated brain area composed of several different subregions densely innervated by serotonin. Interestingly, the BNST exhibits sexual dimorphism: it is neurologically different in males compared to females. To figure out if this brain region contributes to fear or negative emotional responses, I used optogenetics to precisely elevate serotonin availability in the BNST during a fear learning paradigm. I found that increased serotonin release in the BNST enhances fear responses in female, but not male, mice. This is an intriguing and potentially important finding because in the clinical population, women are more than twice as likely to be prescribed SSRIs compared to their male counterparts. 

Now that I have more narrowly defined the behavioral response during times of hyperserotonergic activity in the BNST, I am working to describe the associated neural circuitry. Like all brain regions, the BNST does not exist in isolation. There is a significant projection from the BNST to the central amygdala, a region well known for behavioral fear responses. To understand the communication between these areas, I am implanting electrodes in both regions for awake-behaving electrophysiological data collection. I am continuing to gather electrophysiological data to decipher how the BNST communicates with the central amygdala during times of elevated serotonin availability and if this communication correlates to negative emotional memories.