Dimitrios Kouzoukas
Postdoctoral Scholar at University of Kentucky
*******@*****.***
Summary
Current research focuses on neuro-immune mechanisms of bladder inflammation.
Experience
Postdoctoral Scholar at University of Kentucky
August 2012 - Present (10 months)
Investigating the role of urothelial Protease-Activated Receptors in MIF-mediated bladder inflammation
using a mouse model of Interstitial Cystitis/Painful Bladder Syndrome.
Research Associate (WOC) at Lexington Veterans Affairs Medical Center
August 2012 - Present (10 months)
Internship at University of Kentucky
June 2011 - July 2011 (2 months)
Received training for patch-clamp electrophysiology in hippocampal brain slices.
Graduate Research Assistant / Postdoctoral Scholar at University of Iowa, Graduate College -
Neurobiology (Interdisciplinary Studies)
November 2005 - December 2010 (5 years 2 months)
Studied maturation-acquired alcohol resistance using a cerebellar granule neuronal (CGN) culture model for
Fetal Alcohol Spectrum Disorders. My research showed that 1) alcohol kills developing neurons by
triggering abnormal Ca2+ release from the endoplasmic reticulum via a PLC–IP3 receptor-dependent
mechanism, and that 2) the nitric oxide signaling pathway protects CGN cultures from alcohol exposure by
preventing this endoplasmic reticulum-mediated Ca2+ efflux.
Research Assistant at University of Iowa
2003 - 2005 (2 years)
Performed statistics and data analysis for several studies investigating the neuroanatomical substrates of
emotional processing through MR-based brain morphometry, regional cerebral blood flow responses (PET),
and subjective ratings to emotionally-salient visual stimuli in normal subjects and in patients with lateralized
stroke lesions and in patients with schizophrenia.
Teaching Assistant at University of Iowa
January 2001 - December 2002 (2 years)
For Elementary Psychology, Health Biopsychology, Psychopharmacology, Medical Neuroscience
Teaching Assistant at Loyola University Chicago, Stritch School of Medicine
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January 1999 - May 1999 (5 months)
For Medical Neuroscience
Laboratory Technician at AMCOL International Corp. (Nanocor, Inc)
1996 - 1997 (1 year)
Implemented ASTM standards in the physical characterization of polymer nanocomposites.
Data Entry Operator (Temp) at Northwestern University, School of Education and Social Policy -
Center for Talent Development
1996 - 1996 (less than a year)
Survey data coding and entry.
Organizations
Research Society on Alcoholism
Society for Neuroscience
Bluegrass Chapter of the Society for Neuroscience
Hellenic Professional Society of Illinois
Kentucky Physiological Society
Languages
English (Native or bilingual proficiency)
Greek
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Publications
Intracellular Calcium Plays A Critical Role In The Alcohol-Mediated Death Of Cerebellar Granule
Neurons.
Journal of Neurochemistry February 2013
Authors: Dimitrios Kouzoukas, Guiying Li, Maysaam Takapoo, Moninger Thomas, Ramesh C. Bhalla,
Nicholas J. Pantazis
Alcohol is a potent neuroteratogen that can trigger neuronal death in the developing brain. However, the
mechanism underlying this alcohol-induced neuronal death is not fully understood. Utilizing primary cultures
of cerebellar granule neurons (CGN), we tested the hypothesis that the alcohol-induced increase in
intracellular calcium ([Ca causes the death of CGN. Alcohol induced a dose-dependent (200-800 mg/dl)
neuronal death within 24 hours. Ratiometric Ca + imaging with Fura-2 revealed that alcohol causes a rapid
(one-two minutes), dose-dependent increase in [Ca which persisted for the duration of the experiment (5
or 7 minutes). The alcohol-induced increase in [Ca was observed in Ca + -free media, suggesting
intracellular Ca + release. Pre-treatment of CGN cultures with an inhibitor (2-APB) of the
inositol-triphosphate receptor (IP3R), which regulates Ca + release from the endoplasmic reticulum (ER),
blocked both the alcohol-induced rise in [Ca and the neuronal death caused by alcohol. Similarly,
pre-treatment with BAPTA/AM, a Ca + -chelator, also inhibited the alcohol-induced surge in [Ca and
prevented neuronal death. In conclusion, alcohol disrupts [Ca homeostasis in CGN by releasing Ca +
from intracellular stores, resulting in a sustained increase in [Ca This sustained increase in [Ca may
be a key determinant in the mechanism underlying alcohol-induced neuronal death.
Neuropsychological correlates of normal variation in emotional response to visual stimuli.
The Journal of Nervous and Mental Disease February 2008
Authors: Dimitrios Kouzoukas
Skills & Expertise
Neuroscience
Fluorescence Microscopy
Animal Models
Image Processing
Cell Culture
Molecular Biology
Signal Transduction
Cell Biology
Scientific Writing
ELISA
Western Blotting
qPCR
RT-PCR
Tissue Culture
In Vitro
In Vivo
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Microscopy
Cell Based Assays
Fluorescence
Medical Statistics
SPSS
Education
University of Iowa
PhD, Neurobiology, 2005 - 2010
Activities and Societies: Graduate Student Senate, Orthodox Christian Fellowship
Loyola University of Chicago
BS, Biology / Psychology, 1992 - 1997
Activities and Societies: Loyola University Chicago Honors Program, Alpha Epsilon Delta, Orthodox Christian
Fellowship
Honors and Awards
UNIVERSITY OF IOWA
• Graduate College Summer Fellowship, 2010
• NINDS Neuroscience Training Program Fellowship, 2000–2001
LOYOLA UNIVERSITY CHICAGO
• Presidential Scholarship, 1992–1996
• Honors Program, 1992–1994
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Dimitrios Kouzoukas
Postdoctoral Scholar at University of Kentucky
*******@*****.***
Contact Dimitrios on LinkedIn
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