- Assistant Professor of Neuroscience
- Postdoctoral Research in Neuroscience, Salk Institute for Biological Studies, 2013-2017
- PhD, Illinois State University, 2013
- BS, Illinois State University, 2008
My lab has two overarching goals: To understand the contributions of neuronal circuits to an organism’s behavior and to determine how neuroactive drugs impact these circuits. To this end, I use a multidisciplinary approach including the use of viral tools to control neuronal activity with light (optogenetics), recording of chemicals in the brain (electrochemistry), recording electrical activity of neurons (electrophysiology), and assessing gene expression in neurons (immunohistochemistry), all in the context of behavior.
The particular brain structures I am interested in are neurons that release the neurotransmitter dopamine and their primary target, the striatum. This circuit plays a critical role in reward processing and in selection of behaviors.
These brain regions are also heavily implicated in movement disorders such as Parkinson’s and Huntington’s diseases as well as behavioral dysregulation noted in Obsessive Compulsive Disorder and drug addiction.
Currently, my lab is working to determine:
- how dopamine contributes to the establishment of habitual behaviors such as those noted in drug addiction and Obsessive Compulsive Disorder and
- how a commonly prescribed drug used to treat Parkinson’s disease (levodopa) modulates dopamine signaling and gene expression.
These studies will provide mechanistic insights into how habits develop (and how they can be remediated) and how drugs used to treat Parkinson’s Disease function.
I live in Oberlin with my wife Annie, my two sons Henry and George, and my loyal dog, Jackson.
Neurophysiology, Introductory Neuroscience
Dopamine and action selection, habit formation, drug addiction, dopamine
neurotransmission, Parkinson’s disease, timing (interval judgment)
Howard, C.D., Li, H., Jin, X. Nigrostriatal dopamine biases action selection. Neuron. March 2017. 93(6):1436-1450.
Smith, J.B., Ross, D.L., Klug, J.K., Howard, C.D., Hollon, N.G., Ko, V.I., Hoffman, H., Callaway, C.R., Jin, X. Genetic-based dissection unveils the inputs and outputs of striatal patch and matrix compartments. Neuron. September 2016. 91(5):1069-84.
Robinson, J.D., Howard, C.D., Pastuzyn, E.D., Byers, D.L., Keefe, K.A., Garris, P.A. Methamphetamine-induced neurotoxicity disrupts pharmacologically evoked dopamine transients in the dorsomedial and dorsolateral striatum. Neurotoxicity Research. August 2014. 26(2):152-67.
Bozorgzadeh, B., Covey, D.P., Howard, C.D., Garris, P.A., Mohseni, P. A neurochemical pattern generator SoC with switched-electrode management for single-chip electrical stimulation and 9.3 µW, 78pArms, 400 V/s FSCV sensing. IEEE Journal of Solid State Circuits. April 2014. 49(4): 881-895.
Howard, C.D., Daberkow, D.P., Ramsson, E.R., Keefe, K.A., Garris, P.A. Methamphetamine-induced neurotoxicity disrupts naturally occurring phasic dopamine signaling. European Journal of Neuroscience. July 2013. 38(1): 2078-2088.
Howard, C.D., Pastuzyn, E.D., Barker-Haliski, M.L., Garris, P.A., Keefe, K.A. Striatal gene expression is augmented following phasic-like stimulation of the medial forebrain bundle despite methamphetamine-induced partial dopamine denervation. the Journal of Neurochemistry. May 2013. 125(4): 555-565.
Ramsson, E.S., Howard, C.D., Covey, D.P., Garris, P.A. High doses of amphetamine augment, rather than disrupt, exocytotic dopamine release in the dorsal and ventral striatum of the anesthetized rat. the Journal of Neurochemistry. December 2011. 119(6): 1162-1172.
Howard, C.D., Keefe, K.A., Garris, P.A., Daberkow, D.P. Methamphetamine-induced neurotoxicity decreases phasic, but not tonic, dopaminergic signaling in the rat striatum. the Journal of Neurochemistry. August 2011. 118(4): 668-676.
Covey, D.P., and Howard C.D. Dopaminergic Signaling in Cost-Benefit Analyses: A Matter of Time, Effort, or Uncertainty? the Journal of Neuroscience. February 2011. 31(5): 1561-1562.