About

Shinjae Chung, Ph.D., is an Associate Professor of Neuroscience at the University of Pennsylvania's Perelman School of Medicine. He is affiliated with the Department of Neuroscience and the Graduate Groups in Pharmacology, Cell and Molecular Biology, Bioengineering, and Neuroscience. His research focuses on identifying the molecular and neural mechanisms controlling sleep and understanding how these mechanisms are interconnected with neural circuits regulating emotional states in health and disease. Dr. Chung employs a multidisciplinary approach that includes optogenetics, in vivo electrophysiology, imaging, virus-mediated circuit mapping, and gene profiling to explore neural circuits involved in sleep and neuropsychiatric disorders. His work aims to elucidate the neural circuits and molecular pathways underlying sleep regulation, stress responses, and emotional brain function, contributing to the understanding of neuropsychiatric diseases and sleep disorders.

Research topics

• Neuroscience
• Psychology
• Biology
• Internal medicine
• Endocrinology

Selected publications

• Heart rate and sleep history encode ultradian REM sleep timing

  Current Biology · 2026-03-01

  articleOpen access

  During sleep, the brain alternates between rapid eye movement (REM) and non-REM (NREM) sleep, with recurring REM sleep episodes forming the ultradian sleep cycle, a hallmark of mammalian sleep. However, the mechanisms regulating the ultradian timing of REM sleep remain elusive, underscoring the need for reliable physiological predictors. Here, we developed a machine learning framework to identify features in the electroencephalogram (EEG), electromyogram (EMG), and sleep history that predict the timing of REM sleep in mice. A bidirectional long short-term memory (BiLSTM) network, trained to classify sleep-wake states, embedded EEG and EMG signals into a low-dimensional latent space, revealing slow, ramping dynamics between consecutive REM sleep episodes. Using these latent EEG/EMG features together with preceding sleep history, we predicted the time until the next REM episode. Feature importance analysis identified heart rate in the EMG, combined with sleep history, as a key predictor of REM sleep timing. Under heightened homeostatic pressure for REM sleep, heart rate decayed faster and reached lower levels, whereas pharmacologically elevating heart rate reduced REM sleep. Our findings position heart rate as a physiological marker of REM sleep timing and suggest a close link between cardiovascular regulation and the mechanisms controlling the ultradian sleep cycle.

  PublisherOA PDFDOI

• IL-1b and TNF-a-driven sleep alterations: Neuroimmune mechanisms and behavioral implications

  Brain Behavior & Immunity - Health · 2025-11-06 · 3 citations

  reviewOpen access

  Sleep is a fundamental physiological state essential for immune function, metabolic regulation, and recovery from illness. During infection, sleep patterns are altered in a stereotyped fashion-characterized by increased non-rapid eye movement (NREM) sleep and reduced rapid eye movement (REM) sleep. These sleep changes are not incidental consequences of illness but reflect an evolutionarily conserved neuroimmune adaptation driven by proinflammatory cytokines. In particular, interleukin 1b (IL-1b) and tumor necrosis factor-a (TNFa) modulate sleep by acting directly on central nervous system circuits, including the serotonergic system and homeostatic sleep regulation. In this review, we synthesize current knowledge on how IL-1b and TNFa interact with sleep-regulating networks to alter behavioral state transitions during immune challenge. We also explore the broader clinical relevance of cytokine-driven sleep changes across infectious, psychiatric, and neurodegenerative disorders, and highlight emerging therapeutic opportunities targeting neuroimmune pathways to restore sleep homeostasis. Understanding these interactions is essential for advancing mechanistic insight into sleep regulation and for improving clinical management of inflammation-related sleep disturbances.

  PublisherDOI

• Role of Hypothalamic CRH Neurons in Regulating the Impact of Stress on Memory and Sleep

  Journal of Neuroscience · 2025-06-09 · 2 citations

  articleOpen accessSenior author

  Stress profoundly affects sleep and memory processes. Stress impairs memory consolidation and, similarly, disruptions in sleep compromise memory functions. Yet, the neural circuits underlying stress-induced sleep and memory disturbances are still not fully understood. Here, we show that activation of corticotropin-releasing hormone neurons in the paraventricular nucleus of the hypothalamus (CRH PVN ), similar to acute restraint stress, decreases sleep and impairs memory in a spatial object recognition task in male mice. Conversely, inhibiting CRH PVN neurons during stress reduces stress-induced memory deficits while slightly increasing the amount of sleep. We found that both stress and stimulation of CRH PVN neurons activate neurons in the lateral hypothalamus (LH) and that CRH PVN projections to the LH regulate stress-induced memory deficits and sleep disruptions. Our results suggest that CRH PVN neuronal pathways regulate the adverse effects of stress on memory and sleep—an important step toward improving sleep and ameliorating cognitive deficits associated with stress-related disorders.

  PublisherOA PDFDOI

• Author Response: Homeostatic regulation of REM sleep by the preoptic area of the hypothalamus

  2024-04-03

  peer-reviewOpen accessSenior author

  Rapid-eye-movement sleep (REMs) is characterized by activated electroencephalogram (EEG) and muscle atonia, accompanied by vivid dreams. REMs is homeostatically regulated, ensuring that any loss of REMs is compensated by a subsequent increase in its amount. However, the neural mechanisms underlying the homeostatic control of REMs are largely unknown. Here, we show that GABAergic neurons in the preoptic area of the hypothalamus projecting to the tuberomammillary nucleus (POAGAD2→TMN neurons) are crucial for the homeostatic regulation of REMs. POAGAD2→TMN neurons are most active during REMs, and inhibiting them specifically decreases REMs. REMs restriction leads to an increased number and amplitude of calcium transients in POAGAD2→TMN neurons, reflecting the accumulation of REMs pressure. Inhibiting POAGAD2→TMN neurons during REMs restriction blocked the subsequent rebound of REMs. Our findings reveal a hypothalamic circuit whose activity mirrors the buildup of homeostatic REMs pressure during restriction and that is required for the ensuing rebound in REMs.

  PublisherOA PDFDOI

• Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism

  iScience · 2024-10-30 · 2 citations

  articleOpen accessSenior author

  Sleep disturbances are prevalent in children with autism spectrum disorder (ASD). Strikingly, sleep problems are positively correlated with the severity of ASD symptoms, such as memory impairment. However, the neural mechanisms underlying sleep disturbances and cognitive deficits in ASD are largely unexplored. Here, we show that non-rapid eye movement sleep (NREMs) is fragmented in the 16p11.2 deletion mouse model of ASD. The degree of sleep fragmentation is reflected in an increased number of calcium transients in the activity of locus coeruleus noradrenergic (LC-NE) neurons during NREMs. In contrast, optogenetic inhibition of LC-NE neurons and pharmacological blockade of noradrenergic transmission using clonidine consolidate sleep. Furthermore, inhibiting LC-NE neurons restores memory. Finally, rabies-mediated screening of presynaptic neurons reveals altered connectivity of LC-NE neurons with sleep- and memory-regulatory regions in 16p11.2 deletion mice. Our findings identify a crucial role of the LC-NE system in regulating sleep stability and memory in ASD.

  PublisherDOI

• Homeostatic regulation of rapid eye movement sleep by the preoptic area of the hypothalamus

  eLife · 2024-06-17 · 10 citations

  articleOpen accessSenior author

  Rapid eye movement sleep (REMs) is characterized by activated electroencephalogram (EEG) and muscle atonia, accompanied by vivid dreams. REMs is homeostatically regulated, ensuring that any loss of REMs is compensated by a subsequent increase in its amount. However, the neural mechanisms underlying the homeostatic control of REMs are largely unknown. Here, we show that GABAergic neurons in the preoptic area of the hypothalamus projecting to the tuberomammillary nucleus (POA GAD2 →TMN neurons) are crucial for the homeostatic regulation of REMs in mice. POA GAD2 →TMN neurons are most active during REMs, and inhibiting them specifically decreases REMs. REMs restriction leads to an increased number and amplitude of calcium transients in POA GAD2 →TMN neurons, reflecting the accumulation of REMs pressure. Inhibiting POA GAD2 →TMN neurons during REMs restriction blocked the subsequent rebound of REMs. Our findings reveal a hypothalamic circuit whose activity mirrors the buildup of homeostatic REMs pressure during restriction and that is required for the ensuing rebound in REMs.

  PublisherDOI

• Homeostatic regulation of REM sleep by the preoptic area of the hypothalamus

  eLife · 2024-04-03

  preprintOpen accessSenior author

  Abstract Rapid-eye-movement sleep (REMs) is characterized by activated electroencephalogram (EEG) and muscle atonia, accompanied by vivid dreams. REMs is homeostatically regulated, ensuring that any loss of REMs is compensated by a subsequent increase in its amount. However, the neural mechanisms underlying the homeostatic control of REMs are largely unknown. Here, we show that GABAergic neurons in the preoptic area of the hypothalamus projecting to the tuberomammillary nucleus (POAGAD2→TMN neurons) are crucial for the homeostatic regulation of REMs. POAGAD2→TMN neurons are most active during REMs, and inhibiting them specifically decreases REMs. REMs restriction leads to an increased number and amplitude of calcium transients in POAGAD2→TMN neurons, reflecting the accumulation of REMs pressure. Inhibiting POAGAD2→TMN neurons during REMs restriction blocked the subsequent rebound of REMs. Our findings reveal a hypothalamic circuit whose activity mirrors the buildup of homeostatic REMs pressure during restriction and that is required for the ensuing rebound in REMs.

  PublisherDOI

• Author response: Homeostatic regulation of rapid eye movement sleep by the preoptic area of the hypothalamus

  2024-06-17

  peer-reviewOpen accessSenior author
  PublisherDOI

• Circuit mechanism underlying fragmented sleep and memory deficitsin 16p11.2 deletion mouse model of autism

  Research Square · 2024-03-14 · 1 citations

  preprintOpen access1st authorCorresponding

  Sleep disturbances are prevalent in children with autism spectrum disorder (ASD) and have a major impact on the quality of life. Strikingly, sleep problems are positively correlated with the severity of ASD symptoms, such as memory impairment. However, the neural mechanisms underlying sleep disturbances and cognitive deficits in ASD are largely unexplored. Here, we show that non-rapid eye movement sleep (NREMs) is highly fragmented in the 16p11.2 deletion mouse model of ASD. The degree of sleep fragmentation is reflected in an increased number of calcium transients in the activity of locus coeruleus noradrenergic (LC-NE) neurons during NREMs. Exposure to a novel environment further exacerbates sleep disturbances in 16p11.2 deletion mice by fragmenting NREMs and decreasing rapid eye movement sleep (REMs). In contrast, optogenetic inhibition of LC-NE neurons and pharmacological blockade of noradrenergic transmission using clonidine reverse sleep fragmentation. Furthermore, inhibiting LC-NE neurons restores memory. Rabies-mediated unbiased screening of presynaptic neurons reveals altered connectivity of LC-NE neurons with sleep- and memory regulatory brain regions in 16p11.2 deletion mice. Our findings demonstrate that heightened activity of LC-NE neurons and altered brain-wide connectivity underlies sleep fragmentation in 16p11.2 deletion mice and identify a crucial role of the LC-NE system in regulating sleep stability and memory in ASD.

  PublisherOA PDFDOI

• A hypothalamic circuit mechanism underlying the impact of stress on memory and sleep

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-10-19 · 1 citations

  preprintOpen accessSenior authorCorresponding

  ABSTRACT Stress profoundly affects sleep and memory processes. Stress impairs memory consolidation, and similarly, disruptions in sleep compromise memory functions. Yet, the neural circuits underlying stress-induced sleep and memory disturbances are still not fully understood. Here, we show that activation of CRH PVN neurons, similar to acute restraint stress, decreases sleep and impairs memory in a spatial object recognition task. Conversely, inhibiting CRH PVN neurons during stress reverses stress-induced memory deficits while slightly increasing the amount of sleep. We found that both stress and stimulation of CRH PVN neurons activate neurons in the lateral hypothalamus (LH), and that their projections to the LH are critical for mediating stress-induced memory deficits and sleep disruptions. Our results suggest a pivotal role for CRH PVN neuronal pathways in regulating the adverse effects of stress on memory and sleep, an important step towards improving sleep and ameliorating the cognitive deficits that occur in stress-related disorders.

  PublisherOA PDFDOI

Frequent coauthors

• Franz Weber

  University of Pennsylvania

  89 shared

• Justin Baik

  University of Pennsylvania

  40 shared

• Chang Chu

  Association for Asian Studies

  36 shared

• Stephen Pelz

  36 shared

• Guy S. Alitto

  36 shared

• Jeanne Larsen

  Association for Asian Studies

  36 shared

• Anthony C. Yu

  Stanford University

  36 shared

• Robert N. Smith

  Mississippi Delta Community College

  36 shared

Labs

• Chung LabPI