These findings describe a novel mode of action of neurotransmitter transporters brought about by a naturally occurring human mutation. This mode of action, spontaneous efflux of intracellular neurotransmitter, can now be advanced as a possible reason for the development of multiple brain diseases where altered chemical signaling of classical neurotransmitters is suspected. The A559V mutation that we have described and cell lines expressing the mutation should be beneficial in screening for medications that can selectively halt DA efflux, and similar mutations could be envisaged in other neurotransmitter transporters to establish novel models for efflux-based drug screening. Vanderbilt researchers believe they have established the rationale for a new generation of medications targeting anamalous efflux behaviors in neuronal transporter proteins.

Supplemental Documents
VU06111—A Novel Mechanism Supporting Attention Deficit Hyperactivity Disorder (ADHD)

Inventors
Randy Blakely
Erica Bowton
Aurelio Galli
Michelle Mazei-Robison


CONTACT
Karen Rufus
(615) 322-4295
karen.rufus@vanderbilt.edu

File Number: MKT06111