James Foster awarded multiyear grant from National Institutes of Health

James Foster
James Foster

James Foster, assistant professor in the Department of Biomedical Sciences at the School of Medicine and Health Sciences , has won a two-year award in the amount of $417,000 for a project titled “Dopamine Transporter Palmitoylation.” The grant was awarded by the U.S. Department of Health and Human Services and the National Institutes of Health through a program that promotes the inclusion of undergraduate and graduate students in research.

Palmitoylation is a reversible cellular process wherein lipids (fatty acids) are attached to proteins for the purpose of adjusting protein function and activity. Dr. Foster and his colleagues have identified the dopamine transporter (DAT) as a palmitoylated protein. Dopamine is a chemical “messenger” that sends signals between neurons (nerve cells) and is highly regulated by the dopamine transporter, which transports dopamine back into the neuron from which it was released. Any irregularities that emerge in this process may result in one of several dopamine-related disorders of the central nervous system.

“The proposed research is especially relevant to public health because the dopamine transporter is essential for normal neurotransmission,” explained Foster. “Defects in transporter regulation may be involved with psychiatric and neurodegenerative disorders such as schizophrenia, attention deficit disorder, Parkinson’s, and cocaine and methamphetamine addiction. So figuring out how these processes work in neurons will help us determine how to better treat, if not prevent, these conditions.”

Foster’s previous research studies have found that DAT transport activity is controlled by palmitoylation. Specifically, palmitoylation has been shown to increase DAT activity and can be modified in animals in the presence of addictive drugs such as amphetamine. Dr. Foster’s latest study is expected to substantially advance human understanding of the role of this previously unknown DAT lipid modification on transporter function, and may provide insights into how problems of DAT regulation can lead to neurological disease, including drug abuse.