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INDIVIDUAL RESEARCHER

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

Phone: 518-262-8627
Fax: 518-262-5799

Education

2009 - Toronto Western Hospital [Post Doc Fellowship]
2005 - Ph.D. from University of Toronto
1999 - M.Sc from University of Western Ontario


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.
 
Current Lab Members
Alexander Sutton: PhD candidate
Wilson Yu: PhD candidate
Katie Sheeran: PhD candidate
Autumn Smith: Research Technician
Sujoy Phookan: MD candidate
Manav Kumar: MD candidate
Joannalee Campbell: Post doctoral fellow (Dr. Julie Pilitsis)

 



PubMed Publications

  1. Yu W, Calos M, Pilitsis J, Shin DS (2012). Deconstructing the neural and ionic involvement of seizure-like events in the striatal network. Neurobiology of Disease. Epub ahead of print.


  2. Pushparaj A, Hamani C, Yu W, Shin DS, Nobrega JN, Le Foll B (2012). Electrical stimulation of the insular region attenuates nicotine-taking and nicotine-seeking behaviors. Neuropsychopharmacology. Epub ahead of print.


  3. Sutton A, Yu WJ, Calos ME, Smith AB, Ramirez-Zamora A, Molho ES, Pilitsis JG, Brotchie JM, Shin DS (2012). Deep brain stimulation of the substantia nigra reticulata improves forelimb akinesia in the parkinsonian rat. Journal of Neurophysiology. Epub ahead of print.


  4. Sutton A, Yu WJ, Calos ME, Mueller LE, Berk M, Molho E, Brotchie JM, Carlen PL, Shin DS (2012). Elevated K+ provides an ionic mechanism for deep brain stimulation in the hemiparkinsonian rat. European Journal of Neuroscience. Epub ahead of print.


  5. Huang X, McMahon J, Yang J, Shin D, Huang Y (2012). Rapamycin down-regulates KCC2 expression and increases seizure susceptibility to convulsants in immature rats. Neuroscience. 219:33-47.


  6. Pamenter ME, Hogg DW, Ormond J, Shin DS, Woodin MA, Buck LT (2011). Endogenous GABA(A) and GABA(B) receptor-mediated electrical suppression is critical to neuronal anoxia tolerance. Proceedings of the National Academy of Sciences. 108(27):11274-9.


  7. Zhang ZJ, Koifman J, Shin DS, Ye H, Florez CM, Zhang L, Valiante TA, Carlen PL (2012). Transition to seizure: ictal discharge is preceded by exhausted presynaptic GABA release in the hippocampal CA3 region. Journal of Neuroscience. 32(7):2499-512.


  8. Shin DS, Yu W, Sutton A, Calos M, Puil E, Carlen PL (2011). Isovaline, a rare amino acid, has anti-convulsant properties in two in vitro hippocampal seizure models by increasing interneuronal activity. Epilepsia. 52(11):2084-93.


  9. Shin DS, Yu W, Sutton A, Calos M, Carlen PL (2011). Elevated potassium elicits recurrent surges of large GABAA-receptor mediated post-synaptic currents in hippocampal CA3 pyramidal neurons. Journal of Neurophysiology. 105(3):1185-98.


  10. Shin DS, Yu W, Fawcett A, Carlen PL (2010). Characterizing the persistent CA3 interneuronal spiking activity in elevated extracellular potassium in the young rat hippocampus. Brain Research. 1331:39-50.


  11. Hamani C, Dubiela FP, Soares JCK, Shin D, Bittencourt S, Covolan L, Carlen P, Laxton AW, Hodaie M, Lozano AM, Mello LE, Oliveria MGM (2010). Anterior thalamus deep brain stimulation at high current impairs memory in rats. Experimental Neurology. 225:154-162.


  12. Shin DS, Carlen PL (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.


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


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


  15. Pamenter ME, Shin DS, Buck LT (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.


  16. Wilkie MP, Pamenter ME, Alkabie S, Carapic D, Shin DS, Buck LT (2008). Evidence of Anoxia-Induced Channel Arrest in the Brain of the Goldfish (Carassius auratus). Comparative Biochemistry and Physiology. 148:355-362.


  17. Pamenter ME, Shin DS, Cooray M, Buck LT (2008). Mitochondrial ATP-sensitive K+ channels regulate NMDAR activity in the cortex of the anoxic western painted turtle. Journal of Physiology (London). 586(4):1043-1058.


  18. Pamenter ME, Shin DS, Buck LT (2008). AMPA receptors undergo channel arrest in the anoxic turtle cortex. American Journal of Physiology Regulatory and Integrative Comparative Physiology. 294(2):R606-R613.


  19. Shin DS, Wilkie MP, Pamenter ME, Buck LT (2005). Calcium and protein phosphatase 1/2A attenuate N-methyl-D-aspartate receptor activity in the anoxic turtle cortex. Comparative Biochemistry & Physiology, Part A. 142(1):50-57.


  20. Shin DS, Buck LT (2003). Effect of anoxia and pharmacological anoxia on whole-cell NMDA receptor currents in cortical neurons from the western painted turtle. Physiological and Biochemical Zoology. 76(1):41-51.


  21. Shin DS, Ghai H, Cain S, Buck LT (2003). Gap junctions do not underlie changes in whole-cell conductance in anoxic turtle brain. Comparative Biochemistry and Physiology, Part A. 134(1):179-192.


  22. Buck LT, Shin DS (2002). The role of adenosine in the natural anoxia-tolerance of the freshwater turtle. Trends in Comparative Biochemistry & Physiology. 9:93-116.