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Daewoo Lee

Daewoo Lee, portrait
Life Sciences Building 213

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Ph.D., University of California, Riverside

Courses Taught

  • BIOS 1710 Biological Sciences II: Ecology, Evolution, and Body Systems
  • BIOS 2060 Drugs and the Brain
  • BIOS 3430 Principles of Physiology

Research Interests

  • Lab: Life Sciences Building 210J

The main focus of my research is to understand molecular and cellular mechanisms underlying the information flow between neurons through synapses in the central nervous system. My projects have been primarily involved in two research topics. The first is to study how neurons communicate and thus provide a basis for complex behaviors such as cognition and motor function. In this project, my primary focus has been to elucidate the functional roles of genes and signaling pathways underlying dopamine and serotonin synaptic communication. The second is to investigate the pathophysiological mechanisms of human diseases. Since the synapse is a functional building block of the brain, defects in, or loss of, certain synaptic signaling consequently underlies neural diseases such as Parkinson’s disease.

Drosophila has been the primary model organism used in my research aiming to understand mechanisms underlying brain function and neural diseases. The fruit fly shows a high degree of similarity to mammals in terms of structure and function of the nervous system, but it has a much simpler nervous system. Therefore, the fruit fly nervous system is an excellent model for a reductionist approach to the study of neuronal communication. This system is also amenable to powerful genetic approaches and thus provides a unique opportunity to identify genes involved in fundamental features of brain cell function including neuronal excitability, synaptic transmission, and neuromodulation. In addition, the fruit fly has been frequently used to study the mechanisms underlying neurodegenerative diseases such as Parkinson’s disease. However, there are obvious limitations (e.g., differences in brain anatomy, invertebrate, genetic differences) to the Drosophila models of Parkinson’s disease we have successfully established. Therefore, we are currently developing mammalian models including rat primary neuronal cultures and human DA cell lines (e.g., ReNCell). These additional tools will allow us to test any new findings from Drosophila models in a mammalian/human DA system. I believe this combined approach will function synergistically to expedite the progress of my Parkinson’s disease research.

The following are examples of current active research projects in my lab: (1) Characterization of molecular and cellular mechanisms of biogenic amine (BA) receptor signaling in the Drosophila nervous system, (2) Role of neural circuits in behavior, (3) Dopamine signaling in neurodegeneration and neuroprotection, and (4) L-DOPA-induced dyskinesia (LID) model.

Representative Publications

(Note: * and ** student author(s) from my laboratory: * graduate student, ** undergraduate student)

D. Lee. 2015. Global and local missions of cAMP signaling in neural plasticity, learning and memory. Frontiers in Pharmacology 6:161.

L. Wiemerslage* and D. Lee. 2015. Role of Drosophila calcium channel cacophony in dopaminergic neurodegeneration and neuroprotection. Neuroscience Letters 584:342-346.

C. Qi* and D. Lee. 2014. Pre- and postsynaptic role of dopamine D2 receptor DD2R in Drosophila olfactory associative learning. Biology 3(4): 831-845.

S. Varga**, C. Qi*, E. Podolsky** and D. Lee. 2014. A new Drosophila model to study the interaction between genetic and environmental factors in Parkinson’s disease. Brain Research 1583: 277-286.

L. Wiemerslage*, B.J. Schultz**, A. Ganguly* and D. Lee. 2013. Selective degeneration of dopaminergic neurons by MPP+ and its rescue by D2 autoreceptors in Drosophila primary culture. Journal of Neurochemistry 126 (4): 529-540.

A. Ganguly* and D. Lee. 2013. Suppression of inhibitory GABAergic transmission by cAMP signaling pathway: alterations in learning and memory mutants. European Journal of Neuroscience 37 (9): 1383-1393.