Sean Olson


Sean Olson
Mentor: Dr. Habibeh Khoshbouei
College of Medicine
 
"As an aspiring physician, I feel that there is an obligation to conduct research in order to provide the best standard of patient centered care. I am excited to be involved with research now so that as I am learning how to become an efficient and productive researcher I can contribute to current findings, but also so that I can develop into a physician scientist who helps make discoveries to improve patient care on an even larger scale."

Major

Microbiology & Cell Science

Minor

N/A

Research Interests

  • Neuroscience
  • Drug Addiction
  • Neurodegenerative Disease

Academic Awards

  • University Scholars Program 2016

Organizations

  • Society for Neuroscience

Volunteer

  • Rural Slum Clinic - Faridabad, India
  • UF Health Shands Hospital
  • St. Lucie County Emergency Response

Hobbies and Interests

  • Playing Guitar
  • Cooking

Research Description

Methamphetamine Exposure Alters Membrane Microdomain Distribution of Dopamine Transporter
Psychostimulants such as methamphetamine primarily target dopamine transporter (DAT). The neuronal plasma membrane dopamine transporter (DAT) is essential for the maintenance of dopamine homeostasis in the brain. Impairment of DAT function is implicated in neurodegenerative diseases, drug addiction, and several neuropsychiatric disorders. The long-term goal of my research study is to determine the molecular mechanism underlying methamphetamine regulation of DAT. Membrane proteins are distributed in the plasma membrane; however, this distribution is not random. Membrane proteins are segregated into distinct plasma membrane domains with specialized lipid compositions. These microdomains termed “lipid rafts” or “membrane rafts” are defined as small (10−200 nM) dynamic sterol- and sphingolipid-enriched structures. DAT is distributed in the raft and non-raft membrane microdomains. In my research study I will test the hypothesis that methamphetamine exposure alters membrane microdomain distribution of DAT and subsequently the function of DAT, in the midbrain dopaminergic neurons. Since dysregulation of DAT function is implicated in neurodegenerative diseases, drug addiction, and neuropsychiatric disorders, the results of this work may open new possibilities for development of targeted therapeutic approaches.