We are interested in elucidating how neurons are interconnected and affect each other, and how synapses are modified at the cellular and molecular level. Synapses can vary in their size, strength, and the number.
These differences contribute to learning and memory, beyond the plasticity of neural networks and synapses.

First, we study synaptic plasticity by means of changes in the level of gene expression or circuit specific modulation using viral vectors and transgenic animals. Using genetically modified materials, we can reveal mechanism of spike time dependent plasticity (STDP}, dopamine and it's receptors role in synaptic plasticity or involvement of cell adhesion molecules such as Neuroligin-1. Whole-cell recording is a critical method for observing neural activity in living neurons, and this technique to observe changes of synaptic plasticity. Moreover, we apply behavior experiment using rodents, to find the physiological meaning of alteration in synaptic plasticity.

Second, neurodegenerative diseases or neuropsychiatric disorders appear apparent with failures in synaptic functions and plasticity. Therefore, we pursue the pathophysiology and specific molecular mechanisms of neuronal diseases such as Alzheimer's disease (AD}, autism, or bipolar disorder. Toward this end, we employ variety methodologies, inducing varied behavioral tests, electrophysiological studies in vivo or acute slice, time-lapse imaging of synaptic structures, and optical determination of bimolecular interaction as well as standard biochemical assays.

Third, chronic exposure to drugs of abuse (e.g. cocaine} makes longlasting addictive memory. We investigate electrophysiological, structural and behavioral changes to study long-term changes of reward circuit. Because dopamine Dl and D2 receptor show opposite direction of response in the nucleus accumbens, and they are separately expressed in specific cell type, we are eager to distinguish the functional properties of each type of neurons. BAC transgenic mice (Drdla-EGFP, Drd2-EGFP} enable us to study drug addiction in a celltype specific manner.

Finally, we also conduct systemic approach to study neuronal circuits for functional understanding of various brain areas. For this, we employ a cutting-edge method, opto-or chemo-genetics, which enables us to control the activity of distinct type or group of neurons by optical-or chemical-stimuli and Engram labeling tool, which can label the activated neuronal groups by distinct stimuli. Thus, we can accurately see the role of only optically stimulated neural population or stimuli specific responsible neuronal population in vivo. Currently we are applying these techniques on drug addiction and fear memory research.

• ㆍMolecular mechanisms of synaptic plasticity
• ㆍMechanistic study of cell adhesion molecules
• ㆍPathophysiology of neurodegenerative and psychiatric diseases
• ㆍCell-type specific alteration of neuronal circuitry occurred by drug addiction

• ㆍKo Bum, et al., (2023) Npas4-mediated dopaminergic regulation of safety memory consolidation. Cell Reports 42(7):112678
• ㆍKwon J, et al., (2023) Rewiring of Prelimbic Inputs to the Nucleus Accumbens Core Underlies Cocaine-Induced Behavioral Sensitization. Biological Psychiatry 94(5):378
• ㆍYang YR, et al., (2017) Forebrain-specific ablation of phospholipase Cγ1 causes manic-like behavior. Mol Psychiatry. Mol Psychiatry. 22(10):1473
• ㆍKwon OB, et al., (2015) Dopamine Regulation of Amygdala Inhibitory Circuits for Expression of Learned Fear. Neuron 88(2):378
• ㆍBudreck EC, et al., (2013) Neuroligin-1 controls synaptic abundance of NMDA-type glutamate receptors through extracellular coupling. Proc Natl Acad Sci US A. 110(2):725
• ㆍChoi YB, et al., (2011) Neurexin-neuroligin transsynaptic interaction mediates learning-related synaptic remodeling and long-term facilitation in aplysia. Neuron 70(3):468
• ㆍKim J, et al., (2011) Cell type-specific alterations in the nucleus accumbens by repeated exposures to cocaine. Biol Psychiatry. 69(11):1026
• ㆍJung SY, et al., (2010) Input-specific synaptic plasticity in the amygdala is regulated by neuroligin-1 via postsynaptic NMDA receptors. Proc Natl Acad Sci US A. 107(10):4710
• ㆍKim J, et al., (2008) Neuroligin-1 is required for normal expression of LTP and associative fear memory in the amygdala of adult animals. Proc Natl Acad Sci US A. 105(26):9087

• ㆍB.S., Microbiology, Seoul National University (1992)
• ㆍM.S., Medicine, Seoul National University (1996)
• ㆍPh.D., Neurobiology, Imperial College, University of London (2000)

• ㆍ2000-2005: Postdoctoral Fellow, Columbia Univ., NY, USA.
• ㆍ2001-2004: Research associate, HHMI, NY, USA.
• ㆍ2005-2009: Assistant Professor, POSTECH
• ㆍ2010-2016: Associate professor, POSTECH
• ㆍ2016-Present: Professor, POSTECH

• ㆍFunctional roles of Neuroligin-1 in mature neural circuits
• ㆍElucidation of small GTPase mechanism to long-term memory
• ㆍStructural changes of individual synapses in synaptic plasticity
• ㆍIdentification of pathway-specific alteration of synaptic plasticity
• ㆍDrug addiction mechanism in the basal ganglia circuit
• ㆍAmygdala circuits for fear memory