Jun Hee Kim, Ph.D.
Cellular and Integrative Physiology
Synaptic Physiology, Glia biology, Neurophysiology Research
The goal of my research program is to understand the physiological mechanisms that regulate synaptic function and dysfunction in the auditory nervous system during development, maintenance and disease/injury. After beginning my career as an independent investigator at UTHSCSA in 2010, we have investigated synaptic function and dysfunction related the central myelination in the auditory nervous system, which was successfully funded by the NIH NIDCD (R03 and R01). My lab produced 9 research articles related to demyelination, axon terminal excitability, and synaptic transmission. In the parent R01, we focus on the role of myelination in maintaining synaptic function, and the mechanisms by which myelination supports auditory transmission. Briefly, the ongoing experiments associated with the parent award use a combination of in vivo auditory brainstem response test and patch clamp recordings of auditory neurons in brainstem slices to determine the role of myelination on the functional and structural maturation of synapses, and the mechanisms underlying auditory dysfunction in myelin-deficient auditory brainstem. Our long-term research goal is to determine neurophysiological mechanisms underlying central auditory dysfunctions to improve preventive/ therapeutic strategies for auditory disorders caused by various peripheral hearing deficits (e.g. congenital deafness, noise/trauma-induced hearing loss, or age-related hearing loss). Our published studies in the past funding period show that the loss of condensed myelination increases timing errors and failures in neurotransmission at the calyx of held synapses (Kim et al., 2013 a, b). Changes at the level of individual synapses and alteration in ion channel distribution at axonal domains are associated with delayed and degraded signal transmission along the auditory pathway in a central demyelinating model, Long Evans Shaker rat (Kim et al., 2013b, Berret et al., 2016, Xu et al., 2017). Based on these findings, we will expand our research field to hearing disorders in various neurodegenerative diseases, acoustic trauma, or aging. In the second project, our previous findings lead us to propose that based on their critical needs, neurons and oligodendrocytes (OLs) bi-directionally communicate with high temporal and spatial resolution. However, the mechanisms underlying this process and the cellular factors involved are largely unknown. Our recent study demonstrates a novel excitable OL: A subpopulation of OLs that conducts functional Nav1.2 currents sufficient to evoke APs and the down-regulation of spiking in these excitable OLs impairs myelination in the rat auditory brainstem (Berret et al., 2017, Nat. Communi.). It is striking that a loss of spiking in this excitable subpopulation of OLs had a widespread impact on myelination, suggesting that this subpopulation plays an essential role in promoting myelination as a key coordinator. Our primary goal of this project is identify the oligodendrocytes (OL)-specific signaling molecules, receptors, and ion channels that mediate bidirectional neuron-OL communication. The findings from the proposed studies will identify molecular targets for restoring communication in diseases where neuron-OL interaction is disrupted, including demyelinating diseases and neuropsychiatric disorders.
Sungkyunkwan University Medical School
Sungkyunkwan University Medical School
Food and Nutrition -
Sungshin Women University
Assistant Professor -
UTHSCSA, Physiology, San Antonio
Instruction & Training
- 9/2015 - Present, Post-Doctoral Student Supervision, UTHSCSA
- 8/2015 - Present, Fundamentals of Neuroscience II, The University of Texas Health Science Center
- 4/2015 - Present, Dental Physiology, The University of Texas Health Science Center
- 2/2015 - Present, Ph.D. Dissertations Directed, UTHSCSA
- 8/2014 - Present, Pre-Doctoral Student Supervision, UTHSCSA
- 4/2012 - Present, IBMS 7010-8PP, The University of Texas Health Science Center
- 4/2012 - Present, Fundamentals of Neuroscience I
Research & Grants
Sub-Field of Study: Synaptic transmission, Neuron-Glia interaction, Auditory nervous system
Diseases Relevant: Multiple Sclerosis, Central auditory processing disorder, Autism, Alzheimer
Techniques Used: Electrophysiology, Live-cell Imaging, Immunohistochemistry, RT-PCR
Funding Agency National Institute on Deafness and Other Communication Disorders (NIDCD, NIH) Title Synaptic mechanisms of auditory function and dysfunction Status Active Period 4/2014 - 3/2019 Role Principal Investigator Grant Detail The goal of this study is to determine the fundamental role of myelination in synaptic functions in the auditory nervous system.
These studies will have a significant impact on our understanding of the consequences of synaptic damage following central demyelination and contribute to a rational approach to improving treatments of hearing disorders in multiple sclerosis and other auditory neuropathies.
Funding Agency Southwest National Primate Research Center (SNPRC) Title Synaptic Function in the auditory development in non-human primate Status Active Period 6/2016 - 5/2017 Role Principal Investigator Grant Detail This project will determine synaptic function in the auditory development in non-human primate"
Funding Agency SALSI Clusters in Research Award Title Elucidating social communication deficits in autism Status Active Period 6/2016 - 5/2017 Role Co-Investigator Grant Detail The funds associated with this research enhancement fund are used to initiate a collaboration with Dr. Lee (UTHSCSA) and Dr. Troyer (UTSA). Experiments determined the social communication deficits in autism.
Xu J, Berret E, Kim JH. Development-dependent formation and location of Na channel cluster at the nerve terminal in the auditory nervous system Journal of Neuroscience 2016 Jan;. Berret E, Kim SE, Lee SY, Kushmerick C, Kim JH. Functional and structural changes to the axon terminal caused by myelin degradation Journal of Physiology 2016 Jan;. Lee SY, Kim JH. Mechanisms underlying presynaptic Ca2 transient and vesicular glutamate release at a CNS nerve terminal during in vitro ischemia Journal of Physiology 2015 Jan;593(13):2793-2806.