By Courtney Marshall, PhD

During my undergraduate studies, I had my first opportunity to conduct research in neuroscience when I was selected as an HHMI fellow to study long-term potentiation. As a post-baccalaureate fellow, I continued my research training at the NIA. I expanded my scientific perspective by joining a cardiovascular lab and continued to explore neuroscience research by attending other lab meetings, seminars and poster sessions. Having been exposed to such a variety of topics and techniques, I was drawn to the diverse research program at Drexel's Department of Neurobiology & Anatomy, where I could explore an array of topics and identify the type of neuroscience that piqued my interest.

Drexel's Neuroscience program enabled me to delve into cellular and molecular as well as systems and behavioral neuroscience. Early on I studied the 14-3-3γ protein and neuronal migration. 14-3-3γ is implicated in abnormal cortical layering observed in developmental disorders that also display migration defects. Using RT-PCR analysis, we observed changes in mRNA expression levels of 14-3-3γ in the cortical samples obtained from mice at several developmental time points. Furthermore, upon knocking down the protein using in utero electroporation in conjunction with shRNA, time lapse live imaging demonstrated abnormal migration and morphological patterns in 14-3-3γ deficient neurons. Working on this project exposed me to cellular and molecular techniques, and facilitated my investigation of the relationship between 14-3-3γ mutations and brain morphological disorders.

During the last three years of my PhD, I focused on my thesis project in systems and behavioral neuroscience. My project utilized a pharmacological approach and behavioral techniques to examine the role of the dopamine (DA) D3 receptor (D3R) in a rodent model of mild cognitive impairment in Parkinson's disease (PD-MCI). PD is a movement disorder associated with the progressive degeneration of DA neurons in the mesocortical pathway. Motor symptoms coexist with non-motor symptoms such as cognitive impairment, which correlates with dysfunctional prefrontal mechanisms. Specifically, patients with PD display alterations in the expression of prefrontal D3R whose activity modulates cognitive function. A rodent model of PD-MCI consists of lesions to the mesocortical pathway, thereby disrupting DA signals to the cortical structures responsible for executing cognitive processes. Behavioral assays measuring cognitive function revealed that lesioned rodents display impaired performance, which is ameliorated after pharmacological treatment with a D3R agonist. These findings have been well received and have resulted in two first-author publications.

I enjoyed contributing to the fields of developmental and neurodegenerative research through my work at Drexel. However, my most meaningful experience at Drexel was volunteering to lead a group of high school students at Drexel's Neuroscience Summer Camp. Looking back, I had traversed through high school, college and graduate school without seeing another black person in an advanced scientific position (principal investigator, postdoctoral fellow, etc.). I took pride in mentoring these young, enthusiastic students.

During my time at Drexel I learned that my scientific passion is two-fold: neurodegenerative research and advocacy for a more diverse scientific community. I now work as a postdoctoral fellow at the Center for Neurodegenerative Disease Research at the University of Pennsylvania under the tutelage of Dr. Virginia Lee. During my time here I have seen growth in student diversity at the undergraduate, graduate and postdoctoral levels. I hope to add to this important trend by remaining in academia, where I can serve as a faculty role model and a source of inspiration to my fellow minorities in science.

 
 Back to Top