Sang-Jung Kim
Seoul National University · Neuroscience
About the Lab
Professor Sang-Jung Kim's research lab focuses on the neural and molecular mechanisms underlying brain function, particularly in the context of social behavior, neurovascular regulation, and synaptic plasticity. The lab investigates how early-life experiences shape prefrontal cortical circuits and their subcortical connections, with a focus on the medial prefrontal cortex and nucleus accumbens in social recognition. It also explores the role of calcium signaling in neural progenitor cell differentiation and the function of ion channels such as TRPC in neuronal development. Additionally, the lab contributes to advanced semiconductor device technology, particularly in high-performance InP-based FETs for optoelectronic applications.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15Although medial prefrontal cortex (mPFC) is known to play important roles in social behaviors, how early social experiences affect the mPFC and its subcortical circuit remains unclear. We report that mice singly housed (SH) for 8 weeks after weaning show a social recognition deficit, even after 4 weeks of resocialization. In SH mice, prefrontal infralimbic (IL) neurons projecting to the shell region of nucleus accumbens (NAcSh) show decreased excitability compared with group-housed (GH) mice. NA
Cerebellar Purkinje cells (PCs) are the sole output of the cerebellar cortex and function as key to a variety of learning-related behaviours by integrating multimodal afferent inputs. Intrinsic membrane excitability of neurons determines the input-output relationship, and therefore governs the functions of neural circuits. Cerebellar vermis consists of ten lobules (lobules I-X), and each lobule receives different sensory information. However, lobule-specific differences of electrophysiological p
Circulating endothelial progenitor cells (EPCs) play an important role in physiological and pathological neovascularization and may be involved in attenuating ischemic diseases. This study aimed to characterize circulating EPCs in moyamoya disease (MMD), one of the most common pediatric cerebrovascular diseases. Twenty-eight children with MMD prior to any surgical treatment and 12 healthy volunteers were recruited. Peripheral blood mononuclear cells (PBMNCs) were isolated and cultured in endothe
Neuron–microglia interactions have a crucial role in maintaining the neuroimmune system. The balance of neuroimmune system has emerged as an important process in the pathophysiology of depression. However, how neuron–microglia interactions contribute to major depressive disorders has been poorly understood. Herein, we demonstrated that microglia-derived synaptic changes induced antidepressive-like behavior by using microglia-specific signal transducer and activator of transcription 3 (STAT3) kno
A monolithically integrated p-i-n FET amplifier, fabricated using ion-planted indium-phosphide (InP) JFETs, is described. The vertically integrated structure consists of a vapor-phase epitaxy (VPE)-grown InGaAs photoabsorption layer and a metal-organic-chemical-vapor-disposition (MOCVD)-grown Fe-doped semi-insulating layer. A Zn diffusion was performed to complete the p-i-n photodiode. High-performance fully implanted InP JFETS were used to form the integrated amplifier with a symmetrical design
Store-operated Ca(2+) entry (SOCE) channels are the main pathway of Ca(2+) entry in non-excitable cells such as neural progenitor cells (NPCs). However, the role of SOCE channels has not been defined in the neuronal differentiation from NPCs. Here, we show that canonical transient receptor potential channel (TRPC) as SOCE channel influences the induction of the neuronal differentiation of A2B5(+) NPCs isolated from postnatal-12-day rat cerebrums. The amplitudes of SOCE were significantly higher
For decades, the glial function has been highlighted not only as the 'structural glue', but also as an 'active participant' in neural circuits. Here, we suggest that tumor necrosis factor α (TNF-α), a key inflammatory cytokine, alters the neural activity of the cerebellar Purkinje cells (PCs) by facilitating gliotransmission in the juvenile male rat cerebellum. A bath application of TNF-α (100 ng/ml) in acute cerebellar slices elevates spiking activity of PCs with no alterations in the regularit
We describe a high-performance fully ion-implanted planar InP junction FET fabricated by a shallow (4000-Å) n-channel implant, an n <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">+</sup> source-drain implant to reduce FET series resistance, and a p-gate implant to form a shallow (2000-Å) abrupt p-n junction, followed by a rapid thermal activation. From FET's with gates 2 µm long, a transconductance of 50 mS/mm and an output impedance of 400 Ω.mm ar
Research Areas
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