The dopamine (DA) transporter (DAT) is a sodium symporter (NSS) transporter protein that removes dopamine from the synaptic cleft to the pre-synaptic nerve terminal. DAT is regulated by signal and protein cascade pathways, and thus is trafficked to and from the nerve terminal cell surface to modulate DA uptake. This project investigates the role of calmodulin (CaM) in the signaling pathway affecting DAT trafficking, and focuses on whether CaM is required for PKC-mediated DAT surface expression. DA transport assays using a CaM inhibitor, CGS 9343B, revealed a trend toward CaM’s ability to increase DAT function. Preliminary results suggest that CaM is able to increase DAT function, but whether it affects DAT surface levels is the foundation for further investigations.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Dalton-Petillo, Stephen Neil

Publisher

• Worcester Polytechnic Institute

Identifier

• E-project-011714-151529

Advisor

• Adams, David S.

Year

• 2014

Sponsor

• University of Massachusetts Medical Hospital

Date created

• 2014-01-17

Resource type

• Major Qualifying Project

Major

• Biology & Biotechnology

Rights statement

• In Copyright