Jae-eun Kang Miller
Research Interest
Research Summary
The goal of my laboratory is to determine what goes wrong in neurodegenerative disorders at the circuit level during the behaviors that matter most to the human disease. We tackle this problem using innovative optical tools to image and manipulate brain activity during critical behaviors in mouse models.
One of focuses of my laboratory is Alzheimer’s disease – the most common cause of dementia. Memory loss and cognitive decline in Alzheimer’s disease is likely due to circuit level dysfunction, but the nature of this dysfunction is unknown. We want to address the fundamental question: How does Alzheimer’s disease disrupt circuit activity during learning and memory retrieval? Specifically, we image neuronal ensembles in the hippocampus during spatial navigation and memory tasks using two-photon calcium imaging and freely moving miniature microscope imaging technologies. Furthermore, using simultaneous two-photon imaging and holographic two-photon optogenetic, we aim to determine the causal link between neuronal ensembles and learning and memory.
Another focus of my laboratory is to investigate the neural mechanisms of perceptual learning. Perceptual learning is a progressive improvement in performance on sensory tasks. Investigating the neural mechanisms of perceptual learning will enhance our understanding of plasticity in the adult brain and provide novel insights into learning disability. To tackle this problem, we focus on the primary visual cortex and determine network-level modifications in response to visual stimulation during perceptual learning as well as the modifications in intrinsic activity in the cortex. We also investigate a mechanistic approach to directly stimulate V1 ensembles to accelerate perceptual learning using a holographic two-photon optogenetic.
- BS, 2000 Biology, Kyunghee University in Seoul
- MS, 2003 Biochemistry, Younsei University in Seoul
- PhD, 2009 Neuroscience, Washington University in St Louis
- Postdoc, 2011 Labs of Erik Herzog and Timothy Holy, Washington University in St Louis
- Postdoc, 2020 Lab of Rafael Yuste, Columbia University
Grace Paquelet, Postdoctoral Researcher
Seung Yeon Ko, Postdoctoral Researcher
Fabliha Hussain, Lab manager
Zaheen Hossain, Programmer
Maya Rodriguez, Undergraduate Researcher
Mary Salim, Undergraduate Researcher
Alex Zhang, Undergraduate Researcher
Amber Abud-Romero, Undergraduate Researcher
Nik Patel, Undergraduate Researcher
Miller Kang JE, Miller BR, O’Neil DA, Yuste R. (2022) An increase in spontaneous activity mediates visual habituation. Cell Reports. 39(4):110751.
Carrillo-Reid L, Yang W, Miller Kang JE, Peterka DS, Yuste R. (2017) Imaging and optically manipulating neuronal ensembles. Annu Rev Biophys. 46:271-293.
Karimipanah Y, Ma Z, Miller Kang JE, Yuste R, Wessel R. (2017) Neocortical activity is stimulus- and scale- invariant. PLoS One. 12(5):e0177396.
Yang W, Miller Kang JE, Carrillo-Reid L, Pnevnatikskis E, Paninski L, Yuste R, Peterka D. (2016) Simultaneous multi-plane imaging of neural circuits. Neuron. 89(2):269-84.
Carrillo-Reid L, Miller Kang JE, Hamm JP, Jackson J, Yuste R. (2015) Endogenous Sequential Cortical Activity Evoked by Visual Stimuli. J Neurosci. 35(23):8813-28.
Miller Kang JE, Ayzenshtat I, Carrillo-Reid L, Yuste R. (2014) Visual stimuli recruit intrinsically generated cortical ensembles. PNAS. 111(38):E4053-61.
Miller Kang JE, Granados-Fuentes D, Wang T, Marpegan L, Holy TE, Herzog ED. (2014) Vasoactive intestinal polypeptide mediates circadian rhythms in mammalian olfactory bulb and olfaction. J Neurosci. 34(17):6040-6.
Kang JE, Lim MM, Bateman RJ, Lee JJ, Smyth LP, Cirrito JR, Fujiki N, Nishino S, Holtzman DM. (2009) Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle. Science. 326(5955):1005-7.
Cirrito JR, Kang JE, Lee JY, Stewart FR, Bu G, Mennerick S, Holtzman DM. (2008) Endocytosis is required for synaptic activity-dependent release of amyloid-beta in vivo. Neuron. 58(1):42-51.
Kang JE, Cirrito JR, Dong H, Csernansky JG, Holtzman DM. (2007) Acute stress increases interstitial fluid amyloid-beta via corticotrophin releasing factor (CRF) and neuronal activity. PNAS. 104(25):10673-8.