Cellular and Integrative Physiology

Jun Hee Kim, Ph.D.

Associate Professor

Personal Statement:

To learn more about the lab please click here.


M.S., Medicine, Physiology, Sungkyunkwan University Medical School, South Korea, 2001
Ph.D., Physiology, Sungkyunkwan University Medical School, South Korea, 2004
Postdoctoral fellow, Vollum Institute, Oregon Health Science Center, 2010


I. Synaptic Function and Dysfunction in the Auditory Nervous System

The synapse is the critical structure where neuronal information is transmitted, and presynaptic excitability is crucial for the reliable transmission of this information. However, it is very difficult to study presynaptic activity and vesicular neurotransmitter release directly at CNS nerve terminals, because the sub-micron size of nerve terminals has precluded direct recordings. To study presynaptic properties directly, we take advantage of the calyx of Held, a large terminal in the central auditory system that allows direct recordings. These terminals provide a good model for synaptic transmission because they are a one-to-one synapse (i.e. one terminal to one postsynaptic neuron). Additionally, the role of synaptic transmission in auditory function and dysfunction is easily studied at this synapse. Using patch-clamp recordings and in vivo auditory brainstem response testing, we are studying synaptic activities and plasticity in hearing disorders such as deafness, auditory processing disorder, and those that arise from pre-term birth.

II. Dynamic Communication between Neurons and Oligodendrocytes

Dynamic communication between neurons and myelin-forming oligodendrocytes (OLs) is pivotal in the strength and speed of neurotransmission by influencing myelination in the developing brain. Our recently published studies have created a foothold in understanding communication between neurons and OLs by defining OL excitability in the auditory brainstem. A subpopulation of OLs expresses glutamate receptors and voltage-gated Na+ and Ca2+ channels, which underlie OL depolarization, Na+ current-mediated spiking, and Ca2+ dynamics in OLs (Berret et al., 2017, Barron et al., 2019). A Ca2+ transient in OLs triggers release of brain-derived neurotropic factor (BDNF), important in synaptic strength and plasticity in the auditory brainstem (Jang et al., 2019). We are investigating how neurons and OLs communicate to control activity-dependent myelination in the mammalian brain.


Lab Members

 Mackenna Wollet
Graduate Student
Postdoctoral Fellow
Kaila Nip
Research Associate


Kim EJ, Nip K, Kim JH (2021). Structural refinement of the auditory brainstem neurons in baboons during perinatal development. Front. Cell. Neurosci. in press

Barron T and Kim JH (2020). Preterm birth impedes structural and functional development of cerebellar Purkinje cells in developing baboon cerebellum. Brain Sci. 10(12), 897.

Cong Q, Soteros BM, Wollet M, Kim JH, and Sia GM (2020). The endogenous neuronal complement inhibitor SRPX2 protects against complement-mediated synapse elimination during development. Nat Neurosci. 23, 1067-1078.

Kim EJ, Feng C, Santamaria F, and Kim JH (2019). Impact of auditory experience on structural plasticity of the AIS in the mammalian brain throughout the lifespan. Front. Cell. Neurosci. 13:456. doi: 10.3389/fncel.2019.00456

Barron T and Kim JH (2019). Neuronal input triggers Ca2+ influx through AMPA receptors and voltage-gated Ca2+ channels in oligodendrocytes. Glia. 67(10):1922-1932

Jang M, Xu J, Kim EJ, Gould EA, and Kim JH (2019). Oligodendrocytes regulate presynaptic properties and neurotransmission through BDNF signaling. Under the minor revision, eLife, 8:e42156.

Barron T, Saifetiarova J, Bhat M, and Kim JH (2018). Myelination is critical for synaptic transmission in the deep cerebellar nuclei. Scientific Reports, 8(1):1022.

Berret E, Barron T, Xu J, Debner E, Kim EJ, and Kim JH (2017). Oligodendroglial excitability mediated by glutamatergic inputs and Nav1.2 activation. Nature Communication 8, Article number: 557 (2017) doi:10.1038/s41467-017-00688-0

Xu J, Berret E, Kim JH (2017). Development-dependent formation and location of Na channel cluster at the nerve terminal in the auditory nervous system. J Neurophysol. 117: 582–593

Berret E, Kim SE, Lee SY, Kushmerick C and Kim JH (2016). Functional and structural changes to the axon terminal caused by myelin degradation. J Physiol. doi: 10.1113/JP272205.

Lee SY and Kim JH (2015). Mechanisms underlying presynaptic Ca2+ transient and vesicular glutamate release at a CNS nerve terminal during in vitro ischemia. J Physiol. 593(13): 2793-2806.

Kim SE, Lee SY, Blanco CS and Kim JH (2014). Developmental profiles in intrinsic properties and synaptic function of auditory neurons in term or preterm baboon neonates. J. Neurosci. 34:11399-11404

Kim SE, Turkington K, Kushmerick C and Kim JH (2013). Central dysmyelination reduces the temporal fidelity of synaptic transmission and the reliability of postsynaptic firing during high-frequency stimulation. J Neurophysol. 110(7): 1621-1630.

**Kim JH, Renden R and von Gersdorff H (2013). Dysmyelination of auditory afferent axons increases the jitter of action potential timing during high-frequency firing. J Neurosci. 33(22): 9402-9407, (**Correspondence).

**Kim JH and von Gersdorff H (2012). Suppression of spikes during posttetanic hyperpolarization in auditory neurons: the role of temperature, I(h) currents, and the Na(+)-K(+)-ATPase pump. J Neurophysiol. 108(7): 1924-32. PMID: 22786951 (**Correspondence).

Kim JH, Kushmerick C, von Gersdorff H (2010). Presynaptic resurgent Na+ currents sculpt the action potential waveform and increase firing reliability at a CNS nerve terminal. J Neurosci. 30(46): 15479-15490.

Kim JH and von Gersdorff H (2009). Traffic Jams during vesicle Cycling Lead to Synaptic Depression, Neuron 63(2): 143-145.

Srinivasan G, Kim JH, and von Gersdorff H (2008). The pool of fast releasing vesicles is augmented by myosin light chain kinase inhibition at the calyx of Held synapse. J Neurophysiol. 99(4): 1810-24.

Kim JH, Sizov I, Dobretsov M and von Gersdorff H (2007). Presynaptic Ca2+ buffers control the strength of a fast post-tetanic hyperpolarization mediated by the α3 Na+/K+-ATPase. Nature neuroscience. 10:196-205.