Biomedical Sciences
- Nella Delva
- May 23, 2021
- 4 min read
Updated: Jul 23, 2021
I am a PhD candidate, a neuroscientist in training. I want to take you on this journey with me. I hope to tell you about my experiences, my struggles and share my successes. I also hope to inspired and provide guidance if you're interested in a path similar to mine.
If you're new to the field of biomedical science, it is simply the understanding of biological processes causing disease problems in our body. The goal is to better understand those biological processes in order to help prevent possible viral outbreaks, cure critical genetic diseases, and come up with more efficient treatment for diseases.
My highlights
· A decade of productive research experience in academia with background in cellular, molecular and developmental biology, pre-clinical animal rodent model techniques and handling, target identification and validation.
· Masters in Biological Science with a focus on cellular, molecular and developmental biology (University of South Carolina-Columbia)
· Doctoral Candidate at Florida State University in Biomedical Sciences
· 2 years of teaching experience in biology
· Presentations at national conferences
· Excellent problem-solving, communication, and project management skills
· Successful in collaborative, multi-disciplinary teams, flexible and highly motivated, ability to quickly master new disciplines.

I want to share a piece with you to give you a glance of my experiences as a black immigrant scientist in training on how they see me.
They see me, as if...
They see me as if:
My Black life is invisible
My Black life is disposable
My Black life is unworthy
My Black life is dispensable
They see me as if

My Black life is unimportant
My Black life is replaceable
My Black life is insignificant
They see me as if
My Black life is unbalanced
My Black life is disrespectful
My Black life is irresponsible
My Black life is untrustworthy
They see me as if My Black life is worthless
My Black life is beautiful
My Black life is worthy
My Black life is resilient
My Black life is important
My Black life is strong
My Black life is loving
My Black life is understanding
My Black life is compassionate
My Black life is forgiving
My Black life is intelligent
My Black life is dependable
My Black life is loyal
My Black life is competent
My Black life is successful
AND BEYOND EVERYTHING ELSE I. am. HUMAN and my black life not only matters but is IMPORTANT and NECESSARY for sustainable growth in this world.
Neuroscientist
Major depressive disorder (MDD) also referred as depression affects all age groups; at least 1 in 6 people in the US population is affected every year. MDD produces the greatest decrement in health when compared to other chronic diseases (Kohn et al., 2004; Wainberg et al., 2017). Depression has genetic, epigenetic and environmental contributions; that includes the involvement of chronic and acute stressor as an important environmental contributor in causing MDD (Park et al., 2019; Praag, 2009). In clinical trials, a number of patients do not respond to treatment to newly developed medications and therefore resulting to a high failure rate (Kohn et al., 2005; Wainberg et al., 2017), additionally a significant proportion of MDD patients are “treatment-resistant”. Many existing drug treatments for depression focuses on the neurotransmitter serotonin, however previous studies have also found important roles for the neurotransmitter dopamine (DA) in regulating mood and affect. Dopaminergic systems, in the past decades, have become an important substrate to explore in people suffering from anxiety and depressive disorders since they have been shown to contribute to the underlying pathophysiology changes in mood and cognitive disorders (Grace, 2016).
Recent studies in our lab focus on the effect of neuron specific loss of DA D1 and D2 receptors during brain formation and we have recently discovered that D1 receptors expressed on a specific subpopulation of cerebral cortical interneurons may regulate mood-related behaviors and circuits. We created a model system in which we delete the Drd1 gene from medial ganglionic eminence-derived (MGE) GABAergic neurons, using the Cre-loxP system in laboratory mice; behavioral assessment of those mice showed strong antidepressant-like phenotypes. My proposed aims will assess stress responses in these mice and test the hypothesis that cell-type specific inactivation of D1 receptors in cortical interneurons derived from the Nkx2.1 lineage (MGE-Drd1-cKO mice) alters their cellular and molecular circuitry in the PFC and provides protection from acute and chronic stress.

Innovation
The need for more effective therapeutic target for treatment of MDD remain eminent. Previously discussed studies suggest that cell-specific neuropharmacology strategies could be a possibility (Mondoloni et al., 2012). Cortical interneuron, specifically the subpopulation that develops into fast spiking interneurons may have an important role in both neuropathological processes and in promoting adaptive mechanisms contributing to behavioral and cognitive resilience. In other words, blocking D1 receptors expressed on cortical interneurons, would represent a new and exciting mechanism to treat MDD if well understood.
Goals
Pursue a deeper physiological and neural understanding of the neuroadaptations that accompany Drd1 loss from GABAergic interneurons derived from the embryonic MGE. The resultant data will allow us to develop potentially innovative strategies to use in the development of new and unique therapeutics for the treatment of MDD and/or other mental health conditions.
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