Gwynne Davis - Neuroscience
7154 MRB III
Dopamine (DA) signaling has been shown to be critical for a variety of critical processes, from the ability to execute movement, to reward and motivation When DA signaling is disrupted, a variety of negative consequences can occur. I am interested in the molecular and cellular changes that arise when DA signaling is genetically altered, and how such change affect behavioral output. Specifically, I am examining DA signaling in relation to ADHD, using transgenic mouse models that contain rare knock-in coding variants of the DA transporter (DAT), identified in subjects with ADHD, using behavioral, pharmacological and molecular approaches. Additionally, I am exploring how serotonin signaling responds to alterations in DA signaling and whether alterations could help explain aspects of ADHD linked to impulsivity and motivation.
Raajaram Gowrishankar - Neuroscience
7154 MRB III
The dopamine (DA) transporter (DAT) plays an important role in terminating DA signaling via reuptake of DA into the presynaptic terminal. DAT has been implicated in neuropsychiatric and neurodevelopmental disorders like ADHD and is the target of action for psychostimulants like cocaine and amphetamine. Previous work in the lab has involved the discovery and characterization ofnovel ADHD DAT coding variants. My project in the lab is to elucidate the disruptions in regulation of these novel DAT variants using a heterologous cell expression system assaying for changes in protein-protein interactions and transporter function. Additionally, I am also involved in a biochemical and physiological characterization of a knock-in mouse model expressing one of these ADHD DAT variants, A559V.
Meagan Quinlan - Pharmacology
7144 MRB III
My research explores the molecular underpinnings of serotonin transporter (SERT) regulation. More specifically, I am building on the discovery of multiple, functional SERT coding variants in subjects with autism spectrum disorder (ASD) that display altered regulation through PKG and p38 MAPK-linked pathways. The availability of a mouse model expressing the most common of these variants, SERT Ala56, provides a key opportunity to examine how disrupted SERT function and regulation leads to risk for ASD and other disorders associated with perturbed serotonin signaling.
Cassie Retzlaff - Neuroscience
7148 MRB III
Acetylcholine was the first neurotransmitter to be discovered, and the rate-limiting step in its synthesis is the presynaptic uptake of choline. The high-affinity choline transporter (CHT) is responsible for this uptake. I aim to characterize the regulation of CHT by examining transporter mutants, both natural and engineered, as well as the molecular consequences of CHT dysfunction in vitro and in vivo to gain a more complete picture of how nerve terminals regulate CHT. I hope my work can allow for a greater understanding of diseases that arise from cholinergic dysfunction.
Chelsea Snarrenberg - Neuroscience
7148 MRB III
Dysfunction of dopamine clearance in the synapse has been implicated in several neuropsychiatric diseases such as addiction and schizophrenia. An important regulator of dopamine signaling is the dopamine transporter (DAT), a presynaptic protein responsible for clearing dopamine after release. Using the model system C. elegans, am characterizing novel regulators of DAT using genetic and molecular techniques. A highly conserved, novel regulator of DAT, previously discovered by our lab, is known as swip-10. I seek to further characterize this regulator in C. elegans and elucidate the function of its mammalian ortholog, Mblac1. Given the conservation of dopamine signaling pathways from worm to man, we believe that an intensive study of the regulators of DAT in C. elegans will provide important insights regarding the control of DA signaling in both normal and disease states.