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Research

INDIVIDUAL RESEARCHER

Damian Shin , Ph.D.
Assistant Professor
e-mail: shind@mail.amc.edu


Education

2005 - Ph.D. from University of Toronto


Current Research

The overall goal of my lab is to elucidate the neuronal signaling and information processing of the basal ganglia at the cellular and network level as it pertains to normal brain function and dysfunction. Currently, an understanding of the basal ganglia’s role in motor allowance – whether for its initiation, coordination and/or execution has not been completely determined. To undertake this task my laboratory employs the whole-cell patch-clamp technique or field electrodes on brain slices, in the normal or parkinsonian state, oriented to contain a single or a group of brain regions of the basal ganglia. Furthermore, in order to gain insight into the network properties of the basal ganglia during normal and parkinsonian motor tasks, in vivo recordings in the freely moving animal will also be employed from various basal ganglia nuclei. We hope that the information we obtain from these experiments will develop treatment paradigms for ameliorating the symptoms of Parkinson’s disease. The specific research goals of my lab are outlined below:

1.      Many questions still remain surrounding the mechanisms underlying the modulation and synaptic plasticity of the principle and accessory cells of the basal ganglia in normal and parkinsonian conditions. We will use in vitro approaches to elucidate some of the determinants mediating the modulation of these cells with or without dopaminergic input.  
2.      In order to develop treatment candidates for ameliorating the symptoms of Parkinson’s disease, an understanding of the cellular pathophysiology underlying this disease is essential. Therefore, our research plan will be to examine the oscillatory properties of the basal ganglia under normal and parkinsonian states and identify or characterize how propagation of neuronal communication is impaired throughout the basal ganglia. I will use an in vitro slice model to examine the neuronal communication among all the major nuclei simultaneously in normal and parkinsonian conditions using a multiple-electrode approach (intra- and/or extracellularly). If changes are seen in normal and dopamine-depleted slices, then pharmacological, genetic or molecular approaches will be employed to see how these neuronal modulators affect downstream communication at the cellular level throughout the basal ganglia. 
3.      Currently there is still uncertainty about how information is propagated and consolidated from various cortical regions into and out of the BG. I plan to implant electrodes into the input and output nuclei of the BG in an awake and freely-moving animal to determine if information obtained in this fashion can elucidate how information flow is transmitted for normal and pathophysiological movement function. 
4.      My research interest also focuses on investigating the mechanism(s) underlying the therapeutic effects of deep brain stimulation for treating symptoms of Parkinson’s disease. I plan to begin my research looking at ways in which neurons in the output basal ganglia nuclei respond to deep brain stimulation. I plan to implant electrodes and cannulas into the output basal ganglia nuclei of freely-moving rats and record local field potentials and/or single unit recordings before and after deep brain stimulation, along with cannula-assisted injection of pharmacological modulators of ion channel activity to determine whether any change in efficacy from deep brain stimulation is observable using both electrophysiological recordings and behavourial testing.


PubMed Publications

  1. Shin, D.S. and P.L. Carlen (2008). Enhancement of the hyperpolarization-activated channel mediates the high frequency stimulation and raised K+-induced depression of rat entopeduncular nucleus neuronal activity. Journal of Neurophysiology. 99(5):2203-2219.


  2. Derchansky, M., Shokrollah, J., Mamani, M., Shin, D.S., Sik, A. and P.L. Carlen (2008). Transition to Seizure: A Switch from Phasic Dominant Inhibition to Dominant Excitation. Journal of Physiology (London). 586(2):477-494.


  3. Pamenter, M.E., Shin, D.S., and L.T. Buck (2008). Adenosine mediates NMDA receptor activity in a pertussis toxin-sensitive manner during normoxia but not anoxia in turtle cortex. Brain Research. 1213:27-34.


  4. Shin DS, Samoilova M, Cotic M, Zhang L, Brotchie JM, Carlen PL. High frequency stimulation or elevated K+ depresses neuronal activity in the rat entopeduncular nucleus.Neuroscience. 2007 Oct 12;149(1):68-86.