Departments & Divisions
Currently seeking M.S. & Ph.D. students
Currently not seeking mentees
Yu Shin Kim, Ph.D.
Our research focuses on the function and regulation of sensory modalities including pain, itch, and gentle touch. Special objectives in our research are to understand the cellular and molecular mechanisms of pain by studying neural circuit activities evoked by pain in basal and disease conditions.
Inflammation and nerve injury can result in chronic pain that can seriously challenge daily activities. Pain is mainly mediated by a subset of primary sensory neurons known as nociceptors in Dorsal Root Ganglia (DRG) and Trigeminal Ganglia (TG). How DRG neurons function at a population level under physiological and pathological conditions is not known. Therefore, monitoring the activities of primary nociceptive neurons and axons is crucial to understanding pain mechanisms.
Our research projects include 1) identifying novel plasticity mechanisms underlying the transition from acute to chronic pain, 2) examining the mechanism of Temporomandibular joint disorders (TMD), 3) determining the mechanism of ongoing and evoked pain, 4) characterizing the contributions of central terminal hypersensitivity of DRG neurons to chronic pain, and 5) uncovering the mechanisms by which damages in skin nerve terminals contributes to chronic pain conditions
Diseases associated with our research
Temporomandibular joint disorder, migraine, diabetic neuropathy, neuropathic pain arising from nerve injury, burns and chemotherapeutic drugs, pruritis
Field of Study
Neurobiology and Neuroscience of pain and itch
Scientific Techniques used
We routinely utilize various techniques including mouse genetics, behavioral assays, electrophysiology, biochemistry, molecular biology, pharmacology, immunohistochemistry, and cell culture models in our laboratory. Molecular biology including gene manipulation techniques such as siRNA knockdown and overexpression systems, mouse behavioral assays, mouse genetics, in vivo imaging and electrophysiological recording in primary sensory neurons, spinal cord and brain are very important aspects of the science of understanding and studying sensory biology.
In vivo imaging is one of the ways pain is depicted. Pain signal detection, transmission and modulation can be detected within the cell bodies that reside in DRG and TG. Enabling the expression of a genetically-encoded Ca2+ sensitive indicator (GCaMP) into the DRG and TG neurons has allowed us to successfully detect the primary sensory neuronal activity in the peripheral and central terminals, and their cell bodies as well. We have developed an imaging technique which allows us to simultaneously monitor the activation of >1,800 neurons in the DRG and >2,800 neurons in the TG. By combining the powerful techniques of in vivo multiphoton confocal microscopic imaging, in vivo microscopic miniscope imaging, and electrophysiological recordings in live and freely behaving animals, we have brought cutting edge technology into the pain research field.
In collaboration with many groups in the world, we have acquired and developed powerful transgenic animal tools to study pain and itch and brought those tools to UTHSCSA with us. We now can visualize specific types of primary sensory neurons in live animals.
Field of Study: Neuroscience Sub Field of Study: Pain Specific Field of Study: Chronic pain, chronic Itch Relevant Conditions: Chronic pain, neuropathic pain, inflammation and its pain, temporomandibular joint disorder and its pain, migraine, diabetic neuropathy, neuropathic pain arising from nerve injury, burns and chemotherapeutic drugs or chemotherapy-induced pain, alcohol withdrawal-induced hypersensitivity and pain, arthritis, pruritis Research Techniques: Mouse genetics, behavioral assays, electrophysiology, biochemistry, pharmacogenetics, molecular biology (including siRNA knockdown, in situ hybridization), immunohistochemistry, cell culture models, viral-mediated cell transformation and transduction, Electrophysiology (in vitro and in vivo), Imaging Confocal Microscopy (including in vitro and in vivo imaging). In vitro and in vivo Multiphoton imaging in DRG, TG, spinal cord, and brain. In vivo imaging of different types of cells in freely moving animals.
- 2010 - Ph.D. - Neuroscience - Johns Hopkins University School of Medicine, Baltimore, MD
- 2001 - M.S. - Biochemistry - Kangwon National University, South Korea
- 1999 - B.S. - Biochemistry - Kangwon National University, South Korea
- 04/2019- Present - Tenure-track Associate Professor - University of Texas Health Science Center at San Antonio
- 06/2019-04/2019 - Principal Investigator of Research - Shriners Hospitals for Children-Galveston
- 06/2015-04/2019 - Tenure-track Assistant Professor - University of Texas Medical Branch, Neuroscience and Cell Biology & Anatomy, Galveston, TX
Instruction & Training
- Present, Post-doctoral fellow supervision, University of Texas Health Science Center at San Antonio
Research & Grants
Funding Agency NIH/NIDCR
Title Coupling activation of primary sensory neurons as a novel plasticity mechanism for chronic pain
Period 01/2017 – 12/2021
Role Principal Investigator
Grant Detail The major goals of this project are to investigate new, novel plasticity mechanism of neuronal crosstalk in the dorsal root ganglia (DRG) after injury which is responsible for chronic pain.
TEACHING RESPONSIBILITIES AT UTMB:
Graduate School (GSBS) Courses:
Synapse & Neurodegeneration (NEUR 6221) (2015-2019)
Neurobiology of Disease; Mechanisms of Substance Abuse and Chronic Pain (NEUR 6185) (2015-2019)
Integrative Neuroscience (NEUR 6221) (2015-2019)
Cell Biology (BBSC 6302) (2016-2019)
Biology; Optical Imaging (CELL 6207) (2016-2019)
Medical School Courses:
Gross Anatomy & Radiology, Lecturer & Facilitator of Problem-Based Learning (PBL) (2016-2019)
Neuroscience & Human Behavior, Lecturer & Facilitator of Problem-Based Learning (PBL) (2016-2019)
- Miller RE, Kim YS, Tran PB, Ishihara S, Dong X, Miller RJ, Malfait AM (2018) Visualization of peripheral neuron sensitization in a surgical mouse model of osteoarthritis by in vivo calcium imaging. Arthritis and Rheumatology 70-1: 88-97
- Kim YS*, Anderson M, Park K, Zheng Q, Agarwal A, Gong C, Saijilafu, Young L, He SQ, LaVinka PC, Zhou F, Bergles D, Hanani M, Guan Y, Spray DC, Dong X* (2016) Coupled activation of primary sensory neurons contributes to chronic pain. Neuron 91: 1085-1096 * co-corresponding author.
- Miller RE, Park K, Ishihara S, Kim Y, Miller RJ, Dong X, Malfait AM (2015) In vivo calcium imaging of knee-innervating dorsal root ganglion neurons reveals increased neuronal responsiveness to physical stimuli after dmm surgery. Osteoarthritis and Cartilage. 23(2) A61-62
- Huang CC, Kim YS, Olson WP, Li F, Guo C, Luo W, Huang AJ, Liu Q. A histamine-independent itch pathway is required for allergic ocular itch. (2015) J Allergy Clin Immunol. 6749(15):01343-3
- Pang Z, Sakamoto T, Tiwari V, Kim YS, Yang F, Dong X, Guler AD, Guan Y, Caterina MJ (2015) Selective keratinocyte stimulation is sufficient to evoke nociception in mice. Pain 156(4): 656-65
- Kim YS*, Chu Y*, Han L, Li M, Zhe L, LaVinka PC, Caterina MJ, Ren K, Dubner R, Wei F٭, Dong X٭ (2014) Central terminal sensitization of TRPV1 by descending 5-HT facilitation modulates chronic pain. Neuron 81(4): 873-887 * co-first author. ٭ co-corresponding author.
- Kim YS*, Kang E, Makino Y, Park SJ, Shin JH, Song H, Launay P, Linden DJ* (2013) Characterizing the conductance underlying depolarization-induced slow current (DISC) in cerebellar Purkinje cells. J Neurophysiol 109(4):1174-81. * co-corresponding author.
- Han L, Ma C, Liu Q, Weng H, Cui Y, Tang Z, Kim YS, Nie H, Qu L, Patel KN, Li Z, McNeil B, He S, Guan Y, Xiao B, LaMotte R, and Dong X (2012) A subpopulation of nociceptors specifically linked to itch. Nature Neurosc 16(2):174-82.
- Kim YS, Shin JH, Hall FS, Linden DJ (2009) Dopamine signaling is required for depolarization-induced slow current in cerebellar Purkinje cells. J Neurosci 29(26):8530-38.
- Shin JH*, Kim YS*, Linden DJ (2009) Depolarization-induced slow current in cerebellar Purkinje cells does not require metabotropic glutamate receptor 1. Neuroscience 162(2009):688-693. * co-first author.
- Shin JH, Kim YS, Linden DJ (2008) Dendritic glutamate release produces autocrine activation of mGluR1 in cerebellar Purkinje cells. Proc Natl Acad Sci U S A 105(2):746-50.
- Regan MR, Huang YH, Kim YS, Dykes-Hoberg MI, Jin L, Watkins AM, Bergles DE, Rothstein JD (2007) Variations in promoter activity reveal a differential expression and physiology of glutamate transporters by glia in the developing and mature CNS. J Neurosci 27(25):6607-19.
- Jung SJ, Kim YS, Kim DK, Kim J, Kim SJ (2005) Long-term potentiation of silent synapses in substantia gelatinosa neurons. Neuroreport 16(9):961-965.
- Kim SJ, Kim YS, Yuan JP, Petralia RS, Worley PF, Linden DJ (2003) Activation of the TRPC1 cation channel by metabotropic glutamate receptor mGluR1. Nature 426(6964):285-91.
- Kim YS, Kim SM, Han S (2002) Nitric oxide converts catalase compound II and III to ferricatalase. Bull Korean Chem Soc 23(11): 1664-1666.
- Kim U, Kim YS, Han S (2000) Modulation of cytochrome c-membrane interaction by the physical state of the membrane and the redox state of cytochrome c. Bull Korean Chem Soc 21: 412-418.
- Kim YS, Han S (2000) Superoxide reactivates nitric oxide-inhibited catalase. Biological Chemistry 381: 1269-1271.
- Kim YS, Han S (2000) Nitric oxide protects Cu, Zn-superoxide dismutase from hydrogen peroxide-induced inactivation. FEBS letters 479: 25-28.
Peer-Reviewed Journal Articles
Mouse genetics, behavioral assays, electrophysiology, biochemistry, pharmacogenetics, molecular biology (including siRNA knockdown, in situ hybridization), immunohistochemistry, cell culture models, viral-mediated cell transformation and transduction
Electrophysiology (in vitro and in vivo)
Imaging Confocal Microscopy (including in vitro and in vivo imaging). In vitro and in vivo Multiphoton imaging in DRG, TG, spinal cord, and brain. In vivo imaging of different types of cells in freely moving animals.