Junyoung Kim
VerifiedUniversity of Washington · Asian Languages & Literature
Active 1988–2025
About
Junyoung Kim is a PhD student in Asian Languages and Cultures at the University of Washington, where he also serves as a Teaching Assistant in Korean. His fields of interest include film and cinema, gender and sexuality, Korean, queer politics, and activism. He holds a B.A. in American Studies from the University of California, Berkeley, earned in 2024. In his academic role, he teaches courses such as First-Year Korean, including KOREAN 101 and KOREAN 102, during the Autumn 2025 and Winter 2026 terms. His research and teaching focus on Korean language and culture, with particular attention to issues of gender, sexuality, and activism within Korean society.
Research topics
- Neuroscience
- Psychology
- Biology
- Developmental psychology
- Cognitive psychology
- Ecology
- Psychiatry
- Social psychology
Selected publications
Cell Reports · 2025-07-29 · 4 citations
articleOpen accessSenior authorThis study investigates how amyloid pathology influences hippocampal-prefrontal neural dynamics and decision-making in Alzheimer's disease (AD) using 5XFAD mice, a well-established model system characterized by pronounced early amyloid pathology. Utilizing ecologically relevant "approach food-avoid predator" foraging tasks, we show that 5XFAD mice exhibit persistent risk-taking behaviors and reduced adaptability to changing threat conditions, indicative of impaired decision-making. Multi-regional neural recordings reveal rigid hippocampal CA1 place cell fields, decreased sharp-wave ripple (SWR) frequencies, and disrupted medial prefrontal-hippocampal connectivity, all of which correspond with deficits in behavioral flexibility during spatial risk scenarios. These findings highlight the critical role of SWR dynamics and corticolimbic circuit integrity in adaptive decision-making, with implications for understanding cognitive decline in AD in naturalistic contexts. By identifying specific neural disruptions underlying risky decision-making deficits, this work provides insights into the neural basis of cognitive dysfunction in AD and suggests potential targets for therapeutic intervention.
Distinct disruptions in CA1 and CA3 place cell function in Alzheimer’s disease mice
iScience · 2025-01-09 · 3 citations
articleOpen accessThe hippocampus, a critical brain structure for spatial learning and memory, is susceptible to neurodegenerative disorders such as Alzheimer's disease (AD). Utilizing APPswe/PSEN1dE9 (APP/PS1) mice, we investigated neurophysiological mechanisms underlying AD-associated cognitive impairments by assessing place cell activities in CA1 and CA3 hippocampal subregions, which have distinct yet complementary computational roles. Analyses revealed significant deterioration in spatial representation capabilities of APP/PS1 relative to wild-type (WT) mice. Specifically, CA1 place cells exhibited reduction in coherence and spatial information, while CA3 place cells displayed reduction in place field size. Place cells in both subregions showed disruption in stability and burst firing properties. Furthermore, theta rhythm was significantly attenuated in CA1 place cells of APP/PS1 mice. These findings elucidate that distinct physiological perturbations in CA1 and CA3 place cells, coupled with disrupted hippocampal theta rhythmicity in CA1, potentially orchestrate the impairment of hippocampal-dependent spatial learning and memory in AD pathogenesis.
Bidirectional fear modulation by discrete anterior insular circuits in male mice
eLife · 2024-07-16
preprintOpen accessAbstract The brain’s ability to appraise threats and execute appropriate defensive responses is essential for survival in a dynamic environment. Humans studies have implicated the anterior insular cortex (aIC) in subjective fear regulation and its abnormal activity in fear/anxiety disorders. However, the complex aIC connectivity patterns involved in regulating fear remain under investigated. To address this, we recorded single units in the aIC of freely moving male mice that had previously undergone auditory fear conditioning, assessed the effect of optogenetically activating specific aIC output structures in fear, and examined the organization of aIC neurons projecting to the specific structures with retrograde tracing. Single-unit recordings revealed that a balanced number of aIC pyramidal neurons’ activity either positively or negatively correlated with a conditioned tone-induced freezing (fear) response. Optogenetic manipulations of aIC pyramidal neuronal activity during conditioned tone presentation altered the expression of conditioned freezing. Neural tracing showed that non-overlapping populations of aIC neurons project to the amygdala or the medial thalamus, and the pathway bidirectionally modulated conditioned fear. Specifically, optogenetic stimulation of the aIC-amygdala pathway increased conditioned freezing, while optogenetic stimulation of the aIC-medial thalamus pathway decreased it. Our findings suggest that the balance of freezing-excited and freezing-inhibited neuronal activity in the aIC and the distinct efferent circuits interact collectively to modulate fear behavior.
2024-05-21
peer-reviewOpen accessSenior authorPavlovian fear conditioning research suggests that the interaction between the dorsal periaqueductal gray (dPAG) and basolateral amygdala (BLA) acts as a prediction error mechanism in the formation of associative fear memories. However, their roles in responding to naturalistic predatory threats, characterized by less explicit cues and the absence of reiterative trial-and-error learning events, remain unexplored. In this study, we conducted single-unit recordings in rats during an ‘approach food-avoid predator’ task, focusing on the responsiveness of dPAG and BLA neurons to a looming robot predator. Optogenetic stimulation of the dPAG triggered fleeing behaviors and increased BLA activity in naive rats. Notably, BLA neurons activated by dPAG stimulation displayed immediate responses to the robot, demonstrating heightened synchronous activity compared to BLA neurons that did not respond to dPAG stimulation. Additionally, the use of anterograde and retrograde tracer injections into the dPAG and BLA, respectively, coupled with c-Fos activation in response to predatory threats, indicates that the midline thalamus may play an intermediary role in innate antipredatory defensive functioning.
Author response: Bidirectional fear modulation by discrete anterior insular circuits in male mice
2024-07-16 · 4 citations
peer-reviewOpen accessThe brain’s ability to appraise threats and execute appropriate defensive responses is essential for survival in a dynamic environment. Humans studies have implicated the anterior insular cortex (aIC) in subjective fear regulation and its abnormal activity in fear/anxiety disorders. However, the complex aIC connectivity patterns involved in regulating fear remain under investigated. To address this, we recorded single units in the aIC of freely moving male mice that had previously undergone auditory fear conditioning, assessed the effect of optogenetically activating specific aIC output structures in fear, and examined the organization of aIC neurons projecting to the specific structures with retrograde tracing. Single-unit recordings revealed that a balanced number of aIC pyramidal neurons’ activity either positively or negatively correlated with a conditioned tone-induced freezing (fear) response. Optogenetic manipulations of aIC pyramidal neuronal activity during conditioned tone presentation altered the expression of conditioned freezing. Neural tracing showed that non-overlapping populations of aIC neurons project to the amygdala or the medial thalamus, and the pathway bidirectionally modulated conditioned fear. Specifically, optogenetic stimulation of the aIC-amygdala pathway increased conditioned freezing, while optogenetic stimulation of the aIC-medial thalamus pathway decreased it. Our findings suggest that the balance of freezing-excited and freezing-inhibited neuronal activity in the aIC and the distinct efferent circuits interact collectively to modulate fear behavior.
Author response: Bidirectional fear modulation by discrete anterior insular circuits in male mice
2024-08-01
peer-reviewOpen access2024-08-12 · 1 citations
peer-reviewOpen accessSenior authorElectrophysiological recordings and optogenetics reveal how the dorsal periaqueductal gray and basolateral amygdala interact in antipredatory responses, with a potential intermediary role for the midline thalamus.
Periaqueductal gray activates antipredatory neural responses in the amygdala of foraging rats
eLife · 2024-08-02
preprintOpen accessSenior authorAbstract Pavlovian fear conditioning research suggests that the interaction between the dorsal periaqueductal gray (dPAG) and basolateral amygdala (BLA) acts as a prediction error mechanism in the formation of associative fear memories. However, their roles in responding to naturalistic predatory threats, characterized by less explicit cues and the absence of reiterative trial-and-error learning events, remain unexplored. In this study, we conducted single-unit recordings in rats during an ‘approach food-avoid predator’ task, focusing on the responsiveness of dPAG and BLA neurons to a rapidly approaching robot predator. Optogenetic stimulation of the dPAG triggered fleeing behaviors and increased BLA activity in naive rats. Notably, BLA neurons activated by dPAG stimulation displayed immediate responses to the robot, demonstrating heightened synchronous activity compared to BLA neurons that did not respond to dPAG stimulation. Additionally, the use of anterograde and retrograde tracer injections into the dPAG and BLA, respectively, coupled with c-Fos activation in response to predatory threats, indicates that the midline thalamus may play an intermediary role in innate antipredatory defensive functioning.
Proceedings of the National Academy of Sciences · 2024-03-19 · 8 citations
articleOpen accessWe show that nocturnal aversive stimuli presented to mice while they are eating and drinking outside of their safe nest can entrain circadian behaviors, leading to a shift toward daytime activity. We also show that the canonical molecular circadian clock is necessary for fear entrainment and that an intact molecular clockwork in the suprachiasmatic nucleus, the site of the central circadian pacemaker, is necessary but not sufficient to sustain fear entrainment of circadian rhythms. Our results demonstrate that entrainment of a circadian clock by cyclic fearful stimuli can lead to severely mistimed circadian behavior that persists even after the aversive stimulus is removed. Together, our findings support the interpretation that circadian and sleep symptoms associated with fear and anxiety disorders are, in part, the output of a fear-entrained clock, and provide a mechanistic insight into this clock.
Distinct Disruptions in CA1 and CA3 Place Cell Function in Alzheimer’s Disease Mice
bioRxiv (Cold Spring Harbor Laboratory) · 2024-09-24
preprintOpen accessThe hippocampus, a critical brain structure for spatial learning and memory, is susceptible to neurodegenerative disorders such as Alzheimer's disease (AD). The APPswe/PSEN1dE9 (APP/PS1) transgenic mouse model is widely used to study the pathology of AD. Although previous research has established AD-associated impairments in hippocampal-dependent learning and memory, the neurophysiological mechanisms underlying these cognitive dysfunctions remain less understood. To address this gap, we investigated the activities of place cells in both CA1 and CA3 hippocampal subregions, which have distinct yet complementary computational roles. Behaviorally, APP/PS1 mice demonstrated impaired spatial recognition memory compared to wild-type (WT) mice in the object location test. Physiologically, place cells in APP/PS1 mice showed deterioration in spatial representation compared to WT. Specifically, CA1 place cells exhibited significant reductions in coherence and spatial information, while CA3 place cells displayed a significant reduction in place field size. Both CA1 and CA3 place cells in APP/PS1 mice also showed significant disruptions in their ability to stably encode the same environment. Furthermore, the burst firing properties of these cells were altered to forms correlated with reduced cognition. Additionally, the theta rhythm was significantly attenuated in CA1 place cells of APP/PS1 mice compared to WT. Our results suggest that distinct alteration in the physiological properties of CA1 and CA3 place cells, coupled with disrupted hippocampal theta rhythm in CA1, may collectively contribute to impaired hippocampal-dependent spatial learning and memory in AD.
Recent grants
NIH · $2.6M · 2013
Fear and Natural Risky Decisions in Rats
NIH · $3.9M · 2013–2024
Frequent coauthors
- 43 shared
Jeiwon Cho
Ewha Womans University
- 33 shared
Sanggeon Park
- 32 shared
Eun Joo Kim
University of Washington
- 31 shared
Michael S. Fanselow
Neurobehavioral Systems
- 22 shared
Richard F. Thompson
- 18 shared
Yeowool Huh
Catholic Kwandong University
- 18 shared
Mi-Seon Kong
University of Washington
- 15 shared
Shaowen Bao
University of Arizona
Education
- 1991
Ph.D., Psychology
UCLA
- 1987
B.S., Psychobiology
UCLA
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