Mark Bevan, PhD
m-bevan( at )northwestern.edu
Professor in Physiology
Phd, University of Manchester, England
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Jeremy Atherton, PhD
Research Assistant Professor
PhD, University of Edinburgh, Scotland
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My research to date has primarily focused on the cellular neurophysiology basal ganglia neurons, in particular the intrinsic and synaptic properties of neurons in the subthalamic nucleus (STN) and substantia nigra pars reticulata. My current projects aim to elucidate how the intrinsic and synaptic properties of STN neurons are altered in Parkinson's and Huntington's disease models. To do this I am utilizing classical electrophysiological techniques combined with 2-photon imaging, and optogenetic approaches.

Joshua Callahan, PhD
PhD, Rutgers University

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Excessive synchronization of neuronal activity in the cortico-basal ganglia thalamocortical network is believed to underlie motor symptoms in Parkinson’s disease (PD). Maladaptive alterations in the synaptic and intrinsic properties of neurons in the STN and reciprocally connected external globus pallidus (GPe) are fundamental to the emergence and promotion of synchronous firing in PD. Using an in vivo approach, the goal of my research is to apply optogenetic, pharmacogenetic and genetic tools in the unilateral 6-OHDA lesion mouse model to manipulate activity and restore neuronal firing patterns in order to ameliorate the motor dysfunction associated with PD.

Ryan Kovaleski

Motor dysfunction in Parkinson's disease is associated with an abnormal frequency and pattern of neuronal activity in the cortico-basal ganglia-thalamocortical loop. My project is to determine the origins of this activity pattern in vivo in animals models of Parkinson's disease using simultaneous electrophysiological recording of neuronal activity throughout the cortico-basal ganglia-thalamocortical loop in conjunction with pharmacogenetic and optogenetic approaches.

Asha Lahiri

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My research project focuses on the direct modulation of subthalamic nucleus (STN) activity by substantia nigra dopamine neurons. I will determine whether 1) dopaminergic neuromodulation regulates both autonomous activity and synaptic integration in the STN 2) dopaminergic neuromodulation regulates synaptic plasticity in the STN 3) dopamine neurons co-transmit glutamate and/or GABA. This information will help to determine if nigro-subthalamic inputs promote normal activity in the STN and whether loss of nigro-subthalamic neurons in Parkinson’s disease promotes pathological STN activity.