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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 identify how aberant neuronal signaling and information processing occurs in the basal ganglia at the cellular and network level in Parkinson's disease (PD).  Currently, an understanding of the pathophysiology that contribute to the motor and non-motor complications of this disease remains incomplete. 

To undertake this task, my laboratory employs a variety of electrophysiological techniques  to monitor neuronal activity in brain slices and neuronal activity from multiple brain regions from anesthetized or freely moving normal and parkinsonian animals; the former approach permits us to monitor changes in ion channel activity in neurons while the latter provides information about the neural network and oscillatory changes in PD. We also employ behavioral testing of parkinsonian animals, immunohistochemistry and optogenetics to complement the electrophysiological data.

From our work, we hope that important and innovative findings will emerge that will lead to novel treatment paradigms for managing motor and non-motor symptoms of PD.  The specific research goals of my lab are outlined below:

1.      It's unclear how alteration in synaptic plasticity and information consolidation and propagation of the principle and accessory cells of the basal ganglia manifest in PD. Therefore, we will examine how pathological changes in these processes take place at the synapse and in single neurons. 
 
2.     In order to develop treatment candidates for ameliorating the symptoms of PD, an understanding of the network pathophysiology underlying this disease is important.  Therefore, we will 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 neural network. 
 
3.     My research interest also focuses on investigating the mechanism(s) underlying the therapeutic effects of deep brain stimulation (DBS) for treating symptoms of PD.  We employ electrophysiological and pharmacological techniques to identify how to improve outcomes, minimize stimulation-induced complications and/or expand the efficacy of this approach.  
 
Current Lab Members
Wilson Yu: PhD candidate
Katie Sheeran: PhD candidate
Autumn Smith: Research Technician
Manav Kumar: MD candidate
Ian Walling: Student Intern
Lucy Gee: MD/PhD candidate (co-mentored with Dr. Pilitsis)
Joannalee Campbell: Post doctoral fellow (collaboration with Dr. Pilitsis)

 



PubMed Publications

  1. Yu W, Smith AB, Pilitsis J, Shin D (2013). Isovaline attenuates epileptiform activity and seizure behavior in 4-aminopyridine treated rats. Epilepsy Research. Epub ahead of print.


  2. Yu W, Calos M, Pilitsis J, Shin DS (2013). Deconstructing the neural and ionic involvement of seizure-like events in the striatal network. Neurobiology of Disease. 52:128-136.


  3. Pushparaj A, Hamani C, Yu W, Shin DS, Nobrega JN, Le Foll B (2013). Electrical stimulation of the insular region attenuates nicotine-taking and nicotine-seeking behaviors. Neuropsychopharmacology. 38:690-698.


  4. Sutton A, Yu WJ, Calos ME, Smith AB, Ramirez-Zamora A, Molho ES, Pilitsis JG, Brotchie JM, Shin DS (2013). Deep brain stimulation of the substantia nigra reticulata improves forelimb akinesia in the parkinsonian rat. Journal of Neurophysiology. 109:363-374.


  5. Sutton A, Yu WJ, Calos ME, Mueller LE, Berk M, Molho E, Brotchie JM, Carlen PL, Shin DS (2013). Elevated K+ provides an ionic mechanism for deep brain stimulation in the hemiparkinsonian rat. European Journal of Neuroscience. 37:231-241.


  6. 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.


  7. 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.


  8. 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.


  9. 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.


  10. 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.


  11. 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.


  12. 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.


  13. 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.


  14. 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.


  15. 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.


  16. 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.


  17. 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.


  18. 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.


  19. 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.


  20. 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.


  21. 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.


  22. 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.


  23. 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.