Eric Emmons, PhD

In my research I hope to expand current understanding of the cortex, striatum, and their shared connections in neuropsychiatric disease. Throughout my research, I have focused on cortical regions such as prefrontal cortex and its primary downstream target, the striatum. I am fascinated by the way that neuronal information is processed and transformed as it moves from the cortex to the striatum and beyond in recurring loops that allow us to think, act, and move through the world. These “corticostriatal” circuits are consistently implicated in neuropsychiatric diseases, including Tourette syndrome (TS), OCD, and schizophrenia. In my predoctoral research, I worked in the lab of Dr. Nandakumar Narayanan investigating the role of the prefrontal cortex and striatum in cognition and cognitive dysfunction in rodents. My thesis involved a series of experiments elucidating the respective roles of the prefrontal cortex and striatum as well as the interactions between them during basic cognition. Through these experiments I found corticostriatal representations of cognitive information, reaffirmed the essential top-down influence of the prefrontal cortex on the striatum, and established the sufficiency of prefrontal input to guide cognitive processing in the striatum. In the Pittenger Lab, I will focus on the role of the striatum in the underlying pathophysiology of tic disorders such as TS. I will pursue a couple of different lines of research probing the striatum in tic disorders like TS. In one direction of work, I will combine my background in behavioral electrophysiology with the molecular, cellular, and genetic expertise of the Pittenger lab to interrogate how changes in striatal function lead to repetitive, uncontrollable movements. In another, I will focus on the clinically-motivated histidine decarboxylase (Hdc) genetic mouse model. This model was developed after discovery of a rare but highly penetrant mutation in a family with high incidence of TS. The Hdc-KO mouse has no brain histamine, and the lack of this neurotransmitter leads to inducible tic-like motor behaviors. This phenotype has been extensively characterized by our lab—we know that the lack of histamine affects striatal processing in these mice but we still don’t understand the underlying mechanisms by which this model produces motor stereotypies

resembling tics. My other main line of research will attempt to describe the nuances of the Hdc mouse model as it pertains to tic-like stereotyped movements.