Supervisor: Gregory Funk
Project: Transgenic approaches to understand the life-threatening depression of breathing that accompanies reductions in brain oxygen in prematurity
Bachelor of Science with Honors in Physiology
What's been the best part of your experience so far?
My colleagues and the environment in the Funk Lab have been the best part of my experience. Although I am a summer student, I am treated as a full lab member and given access to every resource I need to be successful. Dr. Funk has an open-door policy which makes him very accessible whenever I run into a problem or have a question. His passion for research and his great (but not unrealistic) expectations for his students motivate me to excel during my studentship. In addition, the lab's technician and graduate students are knowledgeable, accommodating, and patient when I am in the lab and there is always expert advice available when needed. I was initially interested in the Funk Lab because of the fascinating work they do, but it's each member's enthusiasm and kind demeanor that makes this a truly great lab.
What has WCHRI's support through the Foundations for your studentship meant to you?
I am extremely grateful for the support I have received from the Stollery Children's Hospital Foundation through WCHRI. Clinical research lays the foundation for our healthcare system and as a student interested in a health-related career, I think it is vital to be exposed to the research community. Unfortunately, I had not been able to get involved with research in previous summers because I needed to work summer jobs to keep up with day-to-day expenses. This summer, my studentship has helped me with this. I can now pursue my research interests.
Breathing often stops briefly (apnea) in premature infants due to an immature brainstem network that controls the process. During apneas, oxygen levels often fall (hypoxia) triggering a rapid increase in breathing followed by a life-threatening depression of breathing. Adenosine triphosphate (ATP), a molecule that carries energy, is released in the brain during hypoxia and it stimulates breathing, but ATP is metabolized into adenosine (ADO) which, along with other unknown factors, depresses breathing. Thus, the ATP-ADO balance is hypothesized as key in determining the magnitude of the hypoxic respiratory depression. We hypothesized that intracellular ADO metabolism by adenosine kinase (ADK) and/or adenosine deaminase (ADA) regulates this balance. In other brain regions, these enzymes facilitate transport of ADO into cells down its concentration gradient by maintaining low intracellular ADO concentrations. Furthermore, because ADK is immature at birth, we hypothesized that ADO removal mechanisms are reduced at birth, which may underlie the profound hypoxic respiratory depression observed in premature and neonatal mammals. To test these hypotheses, I am evaluating the effects of ADK and ADA inhibition on baseline activity of the breathing network during postnatal development. I predict these interventions to have larger inhibitory effects at later stages of development. If so, then these enzymes may be novel therapeutic targets.