Hey-Kyoung Lee

About

Dr. Hey-Kyoung Lee is a professor of neuroscience at the Johns Hopkins University School of Medicine. Her research focuses on the cellular and molecular changes that occur at synapses to enable memory storage. Her laboratory aims to elucidate the mechanisms underlying cross-modal synaptic plasticity and to expose the events that occur in diseased brains, such as in Alzheimer's disease. She combines techniques such as electrophysiological recording, biochemical/molecular analysis, and imaging to understand the cellular and molecular changes during synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD). Her work includes examining molecular and cellular mechanisms of global homeostatic synaptic plasticity using sensory cortices as model systems, and investigating how sensory loss, such as vision loss, triggers changes in synaptic transmission that may underlie sensory compensation. Dr. Lee's research also involves analyzing alterations in synaptic plasticity mechanisms in mouse models of Alzheimer's disease, in collaboration with other researchers at Johns Hopkins.

Research topics

• Artificial Intelligence
• Psychology
• Computer Science
• Neuroscience
• Cognitive psychology
• Biology
• Physics

Selected publications

• Norepinephrine potentiates and serotonin depresses visual cortical responses by transforming eligibility traces

  Nature Communications · 2022 · 46 citations

  Reinforcement allows organisms to learn which stimuli predict subsequent biological relevance. Hebbian mechanisms of synaptic plasticity are insufficient to account for reinforced learning because neuromodulators signaling biological relevance are delayed with respect to the neural activity associated with the stimulus. A theoretical solution is the concept of eligibility traces (eTraces), silent synaptic processes elicited by activity which upon arrival of a neuromodulator are converted into a…

  PublisherOA PDFDOI

• Cortical and Subcortical Circuits for Cross-Modal Plasticity Induced by Loss of Vision

  Frontiers in Neural Circuits · 2021 · 27 citations

  Senior authorCorresponding

  Cortical areas are highly interconnected both via cortical and subcortical pathways, and primary sensory cortices are not isolated from this general structure. In primary sensory cortical areas, these pre-existing functional connections serve to provide contextual information for sensory processing and can mediate adaptation when a sensory modality is lost. Cross-modal plasticity in broad terms refers to widespread plasticity across the brain in response to losing a sensory modality, and largely…

  PublisherOA PDFDOI

• Metaplasticity framework for cross-modal synaptic plasticity in adults

  Frontiers in Synaptic Neuroscience · 2023-01-06 · 25 citations

  reviewOpen access1st authorCorresponding

  Sensory loss leads to widespread adaptation of neural circuits to mediate cross-modal plasticity, which allows the organism to better utilize the remaining senses to guide behavior. While cross-modal interactions are often thought to engage multisensory areas, cross-modal plasticity is often prominently observed at the level of the primary sensory cortices. One dramatic example is from functional imaging studies in humans where cross-modal recruitment of the deprived primary sensory cortex has b…

  PublisherOA PDFDOI

• Mouse models of <i>SYNGAP1</i> -related intellectual disability

  Proceedings of the National Academy of Sciences · 2023-09-05 · 17 citations

  articleOpen access

  SYNGAP1 is a Ras-GTPase-activating protein highly enriched at excitatory synapses in the brain. De novo loss-of-function mutations in SYNGAP1 are a major cause of genetically defined neurodevelopmental disorders (NDDs). These mutations are highly penetrant and cause SYNGAP1 -related intellectual disability (SRID), an NDD characterized by cognitive impairment, social deficits, early-onset seizures, and sleep disturbances. Studies in rodent neurons have shown that Syngap1 regulates developing exci…

  PublisherOA PDFDOI

• Visual Deprivation Selectively Reduces Thalamic Reticular Nucleus-Mediated Inhibition of the Auditory Thalamus in Adults

  Journal of Neuroscience · 2022-09-07 · 17 citations

  articleOpen accessSenior author

  Sensory loss leads to widespread cross-modal plasticity across brain areas to allow the remaining senses to guide behavior. While multimodal sensory interactions are often attributed to higher-order sensory areas, cross-modal plasticity has been observed at the level of synaptic changes even across primary sensory cortices. In particular, vision loss leads to widespread circuit adaptation in the primary auditory cortex (A1) even in adults. Here we report using mice of both sexes in which cross-m…

  PublisherOA PDFDOI

Recent grants

• Reversible activation of critical period plasticity in visual cortex

  NIH · $3.6M · 2015–2025

• NIH Grant R21NS070645

  NIH · $409k · 2013

• Global Synpatic Plasticity Mechanisms in Visual Cortex

  NIH · $7.9M · 2004–2030

Frequent coauthors

• Richard L. Huganir

  Johns Hopkins Medicine

  67 shared

• Alfredo Kirkwood

  Johns Hopkins University

  55 shared

• Bryce D. Grier

  Allen Institute for Brain Science

  38 shared

• Gabrielle Ewall

  Johns Hopkins Medicine

  36 shared

• Lukas Mesik

  Johns Hopkins Medicine

  28 shared

• Patrick O. Kanold

  Johns Hopkins University

  28 shared

• Samuel Parkins

  Johns Hopkins University

  27 shared

• Ming Gao

  26 shared

Education

• Ph.D., Neuroscience

  Brown University

  1997

• B.S., Biology

  Yonsei University

  1992

Awards & honors

• The Sloan Research Fellowship in 2004
• Junior Faculty Award from the College of Chemical and Life S…
• nominated as one of the "Yonsei 100 Women Leaders" in 2006

Similar researchers at Johns Hopkins University

• Steven L. Salzbergh-191
• Rachel Greenh-114
• Ernesto Freireh-94