BioWave  Vol. 21 No. 5
DGIST Molecular Psychiatry Laboratory 오용석 교수
연구실 홈페이지
실험실 소개 
Mood disorders are largely associated with structural and functional abnormalities within interconnected brain regions and neural circuits, suggesting that changes in emotional information processing are a key component of these disorders. Our research interest focuses on the molecular mechanisms mediating either the abnormal or the beneficial changes in the neural circuit for mood regulation. Through molecular biological, genetic, and genomic approaches, we currently aim to identify the key molecules, neural cell types and their roles in the context of neural circuitry modulation. Our study will help delineate the cell-type specific and further single cell-resolution mechanisms of depression and antidepressant action, and will inform the development of novel therapeutic agents with better therapeutic outcomes.

Neural Cell Types and Circuit in the Hippocampus

Long Term Goal of this Projects
Elucidation of neurobiological mechanisms underlying psychiatric disorders and therapeutics.
Specific Aims:
1. Cell-type specific transcriptional responses to chronic stress exposure and antidepressant medications
2. Molecular basis underlying neuroadaptive changes for major depression and its reversal by antidepressants
3. Illumination of neuroadaptive changes of each cell type within neural circuitry during stress-induced depression and its reversal by antidepressants
4. Genomic anatomy to understand functional heterogeneity of a neuronal cell type in normal and pathological conditions
연구분야 
1. Monoaminergic neurotransmitter as an immediate target of current antidepressant medications
Monoaminergic neurotransmitters including serotonin, norepinephrine, and dopamine, has been closely associated with mood regulation, and thus has been targeted in development of antidepressant drugs. Each neurotransmitter is synthesized by small neuronal subtype in the brain stem area. Those mono-aminergic neurons project its axonal terminals throughout the forebrains. Upon secreted into the synaptic cleft, each neurotransmitter executes its physiological roles via the cognate surface receptor both in the post and the presynaptic density.

The most widely used class of antidepressant SSRI (Selective Serotonin Reuptake Inhibitor) or SNRI (Serotonin-Norepinephrine Reuptake Inhibitor) block those monoamine transporters to elevate the synaptic level of those neurotransmitters. Those antidepressants in clinical use enhance either singly, or in combination, serotonergic, noradrenergic, and, to a lesser extent, dopaminergic neurotransmission.

Monoaminergic neurotransmitter as an immediate target of current antidepressant medications

2. Delayed therapeutic effect of the current antidepressant medication
An enigmatic fact of the current antidepressant medication is its therapeutic delay. Despite its immediate action on increase of serotonin level, the SSRI (selective serotonin reuptake inhibitor) generally take several weeks to display significant therapeutic benefits, in spite of their immediate effect on serotonergic neurotransmission. This therapeutic delay of SSRI medication have suggested importance of slow adaptive changes in neural circuits over prolonged period of drug treatment, possibly via gene regulation and protein translation. However, our knowledge of the molecular mechanisms, underlying therapeutic responses to long-term treatment with SSRIs is yet to be established at the level of key molecules, neuronal cell types, and neural circuitry.

Delayed therapeutic effect of the current antidepressant medication

3. Specific Aims:
Cell-type specific transcriptional responses to chronic stress exposure and antidepressant medications.

Cell-type specific transcriptional responses to chronic stress exposure and antidepressant medications

Molecular basis underlying neuroadaptive changes for major depression and its reversal by antidepressants.

Molecular basis underlying neuroadaptive changes for major depression and its reversal by antidepressants

Genomic anatomy to understand functional heterogeneity of a neuronal cell type in normal and pathological conditions.

Genomic anatomy to understand functional heterogeneity of a neuronal cell type in normal and pathological conditions

연구성과 
Selected Publications(2017년 이후 논문들)

  • Seo-Jin Oh, J. C, Jin-Hyeok Jang, Jeffrey Arace, Minseok Jeong, Changhun Shin, Jeongrak Park, Junghee Jin, Paul Greengard, Yong-Seok Oh (2019)
    Hippocampal mossy cell involvement in behavioral and neurogenic responses to chronic antidepressant treatment.
    Molecular Psychiatry


  • Moon, S. Y. Shin S-A, Oh Y-S,Park H-H,Lee C-S (2018)
    Understanding the Role of the BAI Subfamily of Adhesion G Protein-Coupled Receptors (GPCRs) in Pathological and Physiological Conditions.
    Genes, 9(12):597


  • Shuto, T, Oh. Y-S., et al. (2018)
    Obligatory roles of dopamine D1 receptors in the dentate gyrus in antidepressant actions of a selective serotonin reuptake inhibitor, fluoxetine.
    Molecular Psychiatry


  • Bucher, F.,Oh. Y-S., et al. (2018)
    Interleukin-5 suppresses Vascular Endothelial Growth Factor-induced angiogenesis through STAT5 signaling.
    Cytokine, 110:397-403


  • Leem, E., Oh. Y-S., et al. (2018)
    Upregulation of neuronal astrocyte elevated gene-1 protects nigral dopaminergic neurons in vivo.
    Cell Death & Disease, 9(5):449


  • Kim, S.,Oh. Y-S., et al. (2018)
    Protection of nigral dopaminergic neurons by AAV1 transduction with Rheb(S16H) against neurotoxic inflammation in vivo.
    Experimental & Molecular Medicine, 50:e440


  • Park. J-R Jang. J-H, Oh. S-J, Kim. M-H, Shin. C-H, Jeong. M-S, Heo.K, Park. B-J, Kim. S-R, Oh. Y-S. (2018)
    LPA-induced migration of ovarian cancer cells requires activation of ERM proteins via LPA1 and LPA2.
    Cellular Signalling, 44:138-147


  • Jang, H, Oh, Y-S., et al. (2017)
    Montelukast treatment protects nigral dopaminergic neurons against microglial activation in the 6-hydroxydopamine mouse model of Parkinson's disease.
    Neuroreport


  • Kim, S., Sung, H. J., Lee, J. W., Kim, Y. H., Oh, Y.-S., Yoon, K.-A. Suh, P.-G. (2017)
    C-terminally mutated tubby protein accumulates in aggresomes.
    BMB Reports, 50(1):37-42


  • Kim, S., Oh, Y-S., et al. (2017)
    Beneficial Effects of Silibinin Against Kainic Acid-induced Neurotoxicity in the Hippocampus in vivo.
    Exp Neurobiol., 26(5):266-277


  • Oh, Y.-S., et al. (2017)
    Dynamic relocalization of NHERF1 mediates chemotactic migration of ovarian cancer cells toward lysophosphatidic acid stimulation.
    Experimental & Molecular Medicine, 49:e351


  • OSong M, Mathews CA, Stewart SE, Shmelkov SV, Mezey JG, Rodriguez-Flores JL, Oh Y-S et al.(2017)
    Rare Synaptogenesis-Impairing Mutations in SLITRK5 Are Associated with Obsessive Compulsive Disorder.
    PLoS ONE, 12(1):e0169994
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      지도교수: 오용석

     Research fellow : 장진혁
     Ph.D. Course : 박정락
     MS-Ph.D. integrated course : 오서진, 정민석, 여윤권
     M.S. course : 이준섭
     Researcher : 신창훈, 이소현, 홍교창
    Contact : 053-785-6114(Tel.) /
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