Department of Neuroscience
Professor in the Department of Neuroscience
Phone: (614) 292-4432
Lab Phone: (614) 292-4420
Fax: (614) 688-8742
- Epileptogenesis: molecular mechanisms of cell death and synaptic reorganization
- Huntington’s Disease
- Calcium, CREB and synaptic physiology
- Molecular clock timing mechanisms
- Entrainment of the circadian clock
Research Techniques: Our lab uses a wide variety of cellular, molecular and whole-animal techniques, including quantitative rtPCR, Western blotting, Northern analysis, in situ hybridization, immunocytochemistry, confocal microscopy, viral-mediated gene transfer and behavioral analysis (e.g., memory tests, EEG, seizure activity). A combination of model systems, including primary neuronal cell culture, brain slice and mouse (transgenic and knock-out) are employed.
Cell death and alterations in synaptic architecture may be an underlying event in the development of some forms of epilepsy. Our lab is interested in understanding how these pathophysiological events give rise to the development of temporal lobe epilepsy. Much of our work focuses on the neuroprotective kinase signaling and aberrant axonal growth.
Choi YS, Lee B, Cho H, Reyes S, Pu X-A, Hoyt KR, Obrietan K (2009) CREB is a key regulator of striatal vulnerability in chemical and genetic models of Huntington’s Disease. Neurobiol Dis.: 36: 259-268.
Lee B, Cao R, Choi YS, Cho HY, Rhee AD, Hah CK, Hoyt KR, Obrietan K. (2009) The CREB/CRE transcriptional pathway: protection against oxidative stress-mediated neuronal cell death. J Neurochem. 108:1251-1265.
Our lab is interested in understanding how brief bouts of synaptic communication are translated into long-term alterations in neuronal plasticity. Issues related to cellular kinase pathways, inducible gene expression and neuronal morphology are of particular interest.
Circadian (i.e., 24 hr) rhythms of behavior and physiology are observed in a variety of organisms. In mammals, the suprachiasmatic nuclei (SCN) of the hypothalamus function as the major biological clock. The inherent pacemaker activity of the SCN can be entrained by changes in the environmental light cycle. This allows an animal to synchronize its internal clock with the ever-changing light cycle encountered over a seasonal/yearly basis. Our lab is interested in understanding the molecular and cellular events that underlie both the generation of a biological rhythm and the ability of light to affect clock timing.
Cao R, Lee B, Cho HY, Saklayen S, Obrietan K. (2008) Photic regulation of the mTOR signaling pathway in the suprachiasmatic circadian clock. Mol Cell Neurosci 38:312-324.
Cheng HYM, Alvarez-Saavedra A, Dziema H, Choi YS, Li A, Obrietan K. (2009) Segregation of expression of Period gene homologs in neurons and glia: Possible divergent roles of Period1 and Period2 in the brain. Human Molecular Genetics: 18:3110-3124.
PhD Stanford University
University of Washington